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Hypertension
Other namesArterial hypertension, high blood pressure
Automated arm blood pressure meter showing arterial hypertension (shown by a systolic blood pressure 158 mmHg and diastolic blood pressure 99 mmHg, with a heart rate of 80 beats per minute)
SpecialtyCardiology, Nephrology
SymptomsNone[1]
ComplicationsCoronary artery disease, stroke, heart failure, peripheral arterial disease, vision loss, chronic kidney disease, dementia[2][3][4]
CausesUsually lifestyle and genetic factors[5]
Risk factorsLack of sleep, excess salt, excess body weight, smoking, alcohol[1][5]
Diagnostic methodResting blood pressure in adults
≥ 140/90 mmHg[6]
TreatmentLifestyle changes, medications[7]
Frequency33% (all adults), 16% (diagnosed)
(globally, 2019)[8][9]
Deaths10.4 million; 19% of deaths
(globally, 2019)[8]
Part of a series on
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Hypertension, also known as high blood pressure, is a long-term medical condition in which the blood pressure in the arteries is persistently elevated.[10] High blood pressure usually does not cause symptoms itself.[1] It is, however, a major risk factor for stroke, coronary artery disease, heart failure, atrial fibrillation, peripheral arterial disease, vision loss, chronic kidney disease, and dementia.[2][3][4][11] Hypertension is a major cause of premature death worldwide.[6]

High blood pressure is classified as primary (essential) hypertension or secondary hypertension.[5] About 90–95% of cases are primary, defined as high blood pressure due to non-specific lifestyle and genetic factors.[5] Lifestyle factors that increase the risk include excess salt in the diet, excess body weight, smoking, physical inactivity and alcohol use.[1][5] The remaining 5–10% of cases are categorized as secondary hypertension, defined as high blood pressure due to a clearly identifiable cause, such as chronic kidney disease, narrowing of the kidney arteries, an endocrine disorder, or the use of birth control pills.[5]

Blood pressure is classified by two measurements, the systolic (first number) and diastolic (second number) pressures.[1] For most adults, normal blood pressure at rest is within the range of 100–140 millimeters mercury (mmHg) systolic and 60–90 mmHg diastolic.[12][13] For most adults, high blood pressure is present if the resting blood pressure is persistently at or above 130/80 or 140/90 mmHg.[5][12][13] Different numbers apply to children.[14] Ambulatory blood pressure monitoring over a 24-hour period appears more accurate than office-based blood pressure measurement.[5][10]

Lifestyle changes and medications can lower blood pressure and decrease the risk of health complications.[7] Lifestyle changes include weight loss, physical exercise, decreased salt intake, reducing alcohol intake, and a healthy diet.[5] If lifestyle changes are not sufficient, blood pressure medications are used.[7] Up to three medications taken concurrently can control blood pressure in 90% of people.[5] The treatment of moderately high arterial blood pressure (defined as >160/100 mmHg) with medications is associated with an improved life expectancy.[15] The effect of treatment of blood pressure between 130/80 mmHg and 160/100 mmHg is less clear, with some reviews finding benefit[12][16][17][18] and others finding unclear benefit.[19][20] High blood pressure affects 33% of the population globally.[8] About half of all people with high blood pressure do not know that they have it.[8] In 2019, high blood pressure was believed to have been a factor in 19% of all deaths (10.4 million globally).[8]

Video summary (script)

Signs and symptoms

[edit]

Hypertension is rarely accompanied by symptoms.[1] Half of all people with hypertension are unaware that they have it.[8] Hypertension is usually identified as part of health screening or when seeking healthcare for an unrelated problem.

Some people with high blood pressure report headaches, as well as lightheadedness, vertigo, tinnitus (buzzing or hissing in the ears), altered vision or fainting episodes.[21] These symptoms, however, might be related to associated anxiety rather than the high blood pressure itself.[22]

Long-standing untreated hypertension can cause organ damage with signs such as changes in the optic fundus seen by ophthalmoscopy.[23] The severity of hypertensive retinopathy correlates roughly with the duration or the severity of the hypertension.[21] Other hypertension-caused organ damage include chronic kidney disease and thickening of the heart muscle.[8]

Secondary hypertension

[edit]
Main article: Secondary hypertension

Secondary hypertension is hypertension due to an identifiable cause and may result in certain specific additional signs and symptoms. For example, as well as causing high blood pressure, Cushing's syndrome frequently causes truncal obesity,[24] glucose intolerance, moon face, a hump of fat behind the neck and shoulders (referred to as a buffalo hump), and purple abdominal stretch marks.[25] Hyperthyroidism frequently causes weight loss with increased appetite, fast heart rate, bulging eyes, and tremor. Renal artery stenosis may be associated with a localized abdominal bruit to the left or right of the midline, or in both locations. Coarctation of the aorta frequently causes a decreased blood pressure in the lower extremities relative to the arms, or delayed or absent femoral arterial pulses. Pheochromocytoma may cause abrupt episodes of hypertension accompanied by headache, palpitations, pale appearance, and excessive sweating.[25]

Hypertensive crisis

[edit]
Main article: Hypertensive crisis

Severely elevated blood pressure (equal to or greater than a systolic pressure of 180 mmHg or a diastolic pressure of 120 mmHg) is referred to as a hypertensive crisis.[26] Hypertensive crisis is categorized as either hypertensive urgency or hypertensive emergency, according to the absence or presence of end-organ damage, respectively.[27][28]

In hypertensive urgency, there is no evidence of end-organ damage resulting from the elevated blood pressure. In these cases, oral medications are used to lower blood pressure over 24 to 48 hours gradually.[29]

In a hypertensive emergency, there is evidence of direct damage to one or more organs.[30][31] The most affected organs include the brain, kidney, heart, and lungs, producing symptoms that may include confusion, drowsiness, chest pain, and breathlessness.[29] In a hypertensive emergency, the blood pressure must be reduced more rapidly to stop ongoing organ damage;[29] however, there is a lack of randomized controlled trial evidence for this approach.[31]

Pregnancy

[edit]
Main articles: Gestational hypertension and Pre-eclampsia

Hypertension occurs in approximately 8–10% of pregnancies.[25] Two blood pressure measurements six hours apart of greater than 140/90 mmHg are diagnostic of hypertension in pregnancy.[32] High blood pressure in pregnancy can be classified as pre-existing hypertension, gestational hypertension, or pre-eclampsia.[33] Women who have chronic hypertension before their pregnancy are at increased risk of complications such as premature birth, low birthweight or stillbirth.[34] Women who have high blood pressure and had complications in their pregnancy have three times the risk of developing cardiovascular disease compared to women with normal blood pressure who had no complications in pregnancy.[35][36]

Pre-eclampsia is a serious condition in the second half of pregnancy characterised by increased blood pressure and the presence of protein in the urine.[25] It occurs in about 5% of pregnancies and is responsible for approximately 16% of all maternal deaths globally.[25] Pre-eclampsia also doubles the risk of death of the baby around the time of birth.[25] Usually, there are no symptoms in pre-eclampsia, and it is detected by routine screening. When symptoms of pre-eclampsia occur, the most common are headache, visual disturbance (often "flashing lights"), vomiting, pain over the stomach, and swelling. Pre-eclampsia can occasionally progress to a life-threatening condition called eclampsia, which is a hypertensive emergency and has several serious complications including vision loss, brain swelling, seizures, kidney failure, pulmonary edema, and disseminated intravascular coagulation (a blood clotting disorder).[25][37]

In contrast, gestational hypertension is defined as new-onset hypertension in the second half of pregnancy without protein in the urine.[33]

Exercise during pregnancy is generally safe and may improve outcomes in hypertension during pregnancy,[38] and may prevent gestational hypertension and related complications.[39][40][41]

Children

[edit]

Failure to thrive, seizures, irritability, lack of energy, and difficulty in breathing[42] can be associated with hypertension in newborns and young infants. In older infants and children, hypertension can cause headache, unexplained irritability, fatigue, failure to thrive, blurred vision, nosebleeds, and facial paralysis.[42][43]

Causes

[edit]

Primary hypertension

[edit]
Main article: Essential hypertension

Primary (also termed essential) hypertension results from a complex interaction of genes and environmental factors. More than 2000 common genetic variants with small effects on blood pressure have been identified in association with high blood pressure,[44] as well as some rare genetic variants with large effects on blood pressure.[45] There is also evidence that DNA methylation at multiple nearby CpG sites may link some sequence variation to blood pressure, possibly via effects on vascular or renal function.[46]

Blood pressure rises with aging in societies with a western diet and lifestyle,[47] and the risk of becoming hypertensive in later life is substantial in most such societies.[48] Several environmental or lifestyle factors influence blood pressure. Reducing dietary salt intake lowers blood pressure;[49] as does weight loss,[50] exercise training,[51] vegetarian diets,[52] increased dietary potassium intake[53] and high dietary calcium supplementation.[54] Increasing alcohol intake is associated with higher blood pressure,[55] but the possible roles of other factors such as caffeine consumption,[56] and vitamin D deficiency[57] are less clear. Average blood pressure is higher in the winter than in the summer.[58]

Depression is associated with hypertension[59] and loneliness is also a risk factor.[60] Periodontal disease is also associated with high blood pressure.[61] Arsenic exposure through drinking water is associated with elevated blood pressure.[62] Air pollution is associated with hypertension.[63] Whether these associations are causal is unknown. Gout and elevated blood uric acid are associated with hypertension[64] and evidence from genetic (Mendelian Randomization) studies and clinical trials indicate this relationship is likely to be causal.[65] Insulin resistance, which is common in obesity and is a component of syndrome X (or metabolic syndrome), can cause hyperuricemia and gout[66] and is also associated with elevated blood pressure.[67]

Events in early life, such as low birth weight, maternal smoking, and lack of breastfeeding may be risk factors for adult essential hypertension, although the strength of the relationships is weak and the mechanisms linking these exposures to adult hypertension remain unclear.[68]

Secondary hypertension

[edit]
Main article: Secondary hypertension

Secondary hypertension results from an identifiable cause. Kidney disease is the most common secondary cause of hypertension.[25] Hypertension can also be caused by endocrine conditions, such as Cushing's syndrome, hyperthyroidism, hypothyroidism, acromegaly, Conn's syndrome or hyperaldosteronism, renal artery stenosis (from atherosclerosis or fibromuscular dysplasia), hyperparathyroidism, and pheochromocytoma.[25][69] Other causes of secondary hypertension include obesity, sleep apnea, pregnancy, coarctation of the aorta, excessive eating of liquorice, excessive drinking of alcohol, certain prescription medicines, herbal remedies, and stimulants such as cocaine and methamphetamine.[25][70]

A 2018 review found that any alcohol increased blood pressure in males, while over one or two drinks increased the risk in females.[71]

Pathophysiology

[edit]
Main article: Pathophysiology of hypertension
Determinants of mean arterial pressure
Illustration depicting the effects of high blood pressure

In most people with established essential hypertension, increased resistance to blood flow (total peripheral resistance) accounts for the high pressure while cardiac output remains normal.[72] There is evidence that some younger people with prehypertension or 'borderline hypertension' have high cardiac output, an elevated heart rate and normal peripheral resistance, termed hyperkinetic borderline hypertension.[73] These individuals may develop the typical features of established essential hypertension in later life as their cardiac output falls and peripheral resistance rises with age.[73] Whether this pattern is typical of all people who ultimately develop hypertension is disputed.[74] The increased peripheral resistance in established hypertension is mainly attributable to structural narrowing of small arteries and arterioles,[75] although a reduction in the number or density of capillaries may also contribute.[76]

It is unclear whether or not vasoconstriction of arteriolar blood vessels plays a role in hypertension.[77] Hypertension is also associated with decreased peripheral venous compliance,[78] which may increase venous return, increase cardiac preload and, ultimately, cause diastolic dysfunction. For patients having hypertension, higher heart rate variability (HRV) is a risk factor for atrial fibrillation.[79]

Pulse pressure (the difference between systolic and diastolic blood pressure) is frequently increased in older people with hypertension.[80] This can mean that systolic pressure is abnormally high, but diastolic pressure may be normal or low, a condition termed isolated systolic hypertension.[81] The high pulse pressure in elderly people with hypertension or isolated systolic hypertension is explained by increased arterial stiffness, which typically accompanies aging and may be exacerbated by high blood pressure.[82]

Many mechanisms have been proposed to account for the rise in peripheral resistance in hypertension. Most evidence implicates either disturbances in the kidneys' salt and water handling (particularly abnormalities in the intrarenal renin–angiotensin system)[83] or abnormalities of the sympathetic nervous system.[84] These mechanisms are not mutually exclusive, and both likely contribute to some extent in most cases of essential hypertension. It has also been suggested that endothelial dysfunction and vascular inflammation may also contribute to increased peripheral resistance and vascular damage in hypertension.[85][86] Interleukin 17 has garnered interest for its role in increasing the production of several other immune system chemical signals thought to be involved in hypertension such as tumor necrosis factor alpha, interleukin 1, interleukin 6, and interleukin 8.[87]

Excessive sodium or insufficient potassium in the diet leads to excessive intracellular sodium, which contracts vascular smooth muscle, restricting blood flow and so increases blood pressure.[88][89] Non-modulating essential hypertension is a form of salt-sensitive hypertension, where sodium intake does not modulate either adrenal or renal vascular responses to angiotensin II.[90] They make up 25% of the hypertensive population.[91]

Diagnosis

[edit]

Hypertension is diagnosed based on persistently high resting blood pressure. Elevated blood pressure measurements on at least two separate occasions are required for a diagnosis of hypertension.[12][13][6]

Measurement technique

[edit]

For an accurate diagnosis of hypertension to be made, proper blood pressure measurement technique must be used.[92] Improper measurement of blood pressure is common and can change the blood pressure reading by up to 10 mmHg, which can lead to misdiagnosis and misclassification of hypertension.[92] The correct blood pressure measurement technique involves several steps. Proper blood pressure measurement requires the person whose blood pressure is being measured to sit quietly for at least five minutes, which is then followed by the application of a properly fitted blood pressure cuff to a bare upper arm.[92] The person should be seated with their back supported, feet flat on the floor, and with their legs uncrossed.[92] The person whose blood pressure is being measured should avoid talking or moving during this process.[92] The arm being measured should be supported on a flat surface at the level of the heart.[92] Blood pressure measurement should be done in a quiet room so the medical professional checking the blood pressure can hear the Korotkoff sounds while listening to the brachial artery with a stethoscope for accurate blood pressure measurements.[92][93] The blood pressure cuff should be deflated slowly (2–3 mmHg per second) while listening for the Korotkoff sounds.[93] The bladder should be emptied before a person's blood pressure is measured since this can increase blood pressure by up to 15/10 mmHg.[92] Multiple blood pressure readings (at least two) spaced 1–2 minutes apart should be obtained to ensure accuracy.[93] Ambulatory blood pressure monitoring over 12 to 24 hours is the most accurate method to confirm the diagnosis.[94] An exception to this is those with very high blood pressure readings, especially when there is poor organ function.[95]

With the availability of 24-hour ambulatory blood pressure monitors and home blood pressure machines, the importance of not wrongly diagnosing those who have white coat hypertension has led to a change in protocols. In the United Kingdom, the current best practice is to follow up a single raised clinic reading with ambulatory measurement, or, less ideally, with home blood pressure monitoring over 7 days.[95] The United States Preventive Services Task Force also recommends getting measurements outside of the healthcare environment.[94] Pseudohypertension in the elderly or noncompressibility artery syndrome may also require consideration. This condition is believed to be due to calcification of the arteries, resulting in abnormally high blood pressure readings with a blood pressure cuff, while intra-arterial measurements of blood pressure are normal.[96] Orthostatic hypertension is when blood pressure increases upon standing.[97]

Other investigations

[edit]

Once the diagnosis of hypertension has been made, further testing may be performed to find secondary hypertension, identify comorbidities such as diabetes, identify hypertension-caused organ damage such as chronic kidney disease or thickening of the heart muscle, and for cardiovascular disease risk stratification.[98]

Secondary hypertension is more common in preadolescent children, with most cases caused by kidney disease. Primary or essential hypertension is more common in adolescents and adults and has multiple risk factors, including obesity and a family history of hypertension.[99]

Initial assessment upon diagnosis of hypertension should include a complete history and physical examination. The World Health Organization suggests the following initial tests: serum electrolytes, serum creatinine, lipid panel, HbA1c or fasting glucose, urine dipstick and electrocardiogram (ECG/EKG).[98] Serum creatinine is measured to assess for the presence of kidney disease, which can be either the cause or the result of hypertension.[30] eGFR can also provide a baseline measurement of kidney function that can be used to monitor for side effects of certain anti-hypertensive drugs on kidney function. Testing of urine samples for protein is used as a secondary indicator of kidney disease. Lipid panel and glucose tests are done to identify comorbidities such as diabetes and hyperlipidemia and for cardiovascular risk stratification. Electrocardiogram testing is done to check for evidence that the heart is under strain from high blood pressure, such as thickening of the heart muscle or whether the heart has experienced a prior minor disturbance, such as a silent heart attack.

Classification in adults

[edit]

The circumstances of measurement can influence blood pressure measurements.[100] Guidelines use different thresholds for office (also known as clinic), home (when the patient measures their blood pressure at home), and ambulatory blood pressure (using an automated device over 24 hours).[100]

Blood pressure classifications
Categories Systolic blood pressure, mmHg and/or Diastolic blood pressure, mmHg
Method Office Home 24h ambulatory Office Home 24h ambulatory
American College of Cardiology/American Heart Association (2017)[101]
Normal <120 <120 <115 and <80 <80 <75
Elevated 120–129 120–129 115–124 and <80 <80 <75
Hypertension, stage 1 130–139 130–134 125–129 or 80–89 80–84 75–79
Hypertension, stage 2 ≥140 ≥135 ≥130 or ≥90 ≥85 ≥80
European Society of Cardiology (2024)[100]
Non-elevated <120 <120 <115 and <70 <70 <65
Elevated 120–139 120–135 115–129 and 70–89 70–85 65–79
Hypertension ≥140 ≥135 ≥130 or ≥90 ≥85 ≥80
European Society of Hypertension/International Society of Hypertension (2023)[13]
Optimal <120 — — and <80 — —
Normal 120–129 — — and/or 80–84 — —
High normal 130–139 — — and/or 85–89 — —
Hypertension, grade 1 140–159 ≥135 ≥130 and/or 90–99 ≥85 ≥80
Hypertension, grade 2 160–179 — — and/or 100–109 — —
Hypertension, grade 3 ≥180 — — and/or ≥110 — —

Children

[edit]

Hypertension occurs in around 0.2 to 3% of newborns; however, blood pressure is not measured routinely in healthy newborns.[43] Hypertension is more common in high risk newborns. A variety of factors, such as gestational age, postconceptional age, and birth weight need to be taken into account when deciding if blood pressure is normal in a newborn.[43]

Hypertension, defined as elevated blood pressure over several visits, affects 1% to 5% of children and adolescents and is associated with long-term risks of ill-health.[102] Blood pressure rises with age in childhood, and, in children, hypertension is defined as an average systolic or diastolic blood pressure on three or more occasions equal or higher than the 95th percentile appropriate for the sex, age, and height of the child. High blood pressure must be confirmed on repeated visits, however, before characterizing a child as having hypertension.[102] In adolescents, it has been proposed that hypertension is diagnosed and classified using the same criteria as in adults.[102]

Prevention

[edit]

Much of the disease burden of high blood pressure is experienced by people who are not labeled as hypertensive.[103] Consequently, population strategies are required to reduce the consequences of high blood pressure and reduce the need for antihypertensive medications. Lifestyle changes are recommended to lower blood pressure.

Recommended lifestyle changes for the prevention of hypertension include:

  • maintain normal body weight for adults (e.g. body mass index below 25 kg/m2)[13]
  • reduce dietary sodium intake to <100 mmol/day (<6 g of salt (sodium chloride) or <2.4 g of sodium per day)[13]
  • engage in regular aerobic physical activity with moderate intensity (minimum 150 minutes per week)[13]
  • limit alcohol consumption,[13] max 1 drink for women and 2 for men per day[6]
  • consume a diet rich in whole grains, fruits, and vegetables,[13] such as the DASH diet[13]
  • not smoking[13]
  • stress reduction and management,[13] e.g. by meditation and yoga[13]

Effective lifestyle modification may lower blood pressure as much as an individual antihypertensive medication. Combinations of two or more lifestyle modifications can achieve even better results.[103] There is considerable evidence that reducing dietary salt intake lowers blood pressure, but whether this translates into a reduction in mortality and cardiovascular disease remains uncertain.[104] Estimated sodium intake ≥6 g/day and <3 g/day are both associated with high risk of death or major cardiovascular disease, but the association between high sodium intake and adverse outcomes is only observed in people with hypertension.[105] Consequently, in the absence of results from randomized controlled trials, the wisdom of reducing levels of dietary sodium intake below 3 g/day has been questioned.[104] ESC guidelines mention periodontitis is associated with poor cardiovascular health status.[106]

The value of routine screening for hypertension is debated.[107][108][109] In 2004, the National High Blood Pressure Education Program recommended that children aged 3 years and older have blood pressure measurement at least once at every health care visit[102] and the National Heart, Lung, and Blood Institute and American Academy of Pediatrics made a similar recommendation.[110] However, the American Academy of Family Physicians[111] supports the view of the U.S. Preventive Services Task Force that the available evidence is insufficient to determine the balance of benefits and harms of screening for hypertension in children and adolescents who do not have symptoms.[112][113] The US Preventive Services Task Force recommends screening adults 18 years or older for hypertension with office blood pressure measurement.[109][114]

Management

[edit]
Main article: Management of hypertension

According to one review published in 2003, reduction of the blood pressure by 5 mmHg can decrease the risk of stroke by 34%, of ischemic heart disease by 21%, and reduce the likelihood of dementia, heart failure, and mortality from cardiovascular disease.[115]

Target blood pressure

[edit]
See also: Comparison of international blood pressure guidelines

Various expert groups have produced guidelines regarding how low the blood pressure target should be when a person is treated for hypertension. These groups recommend a target below the range of 140–160 / 90–100 mmHg for the general population.[13][14][116][117] Cochrane reviews recommend similar targets for subgroups such as people with diabetes[118] and people with prior cardiovascular disease.[119] Additionally, Cochrane reviews have found that for older individuals with moderate to high cardiovascular risk, the benefits of trying to achieve a lower-than-standard blood pressure target (at or below 140/90 mmHg) are outweighed by the risk associated with the intervention.[120] These findings may not be applicable to other populations.[120]

Many expert groups recommend a slightly higher target of 150/90 mmHg for those somewhere between 60 and 80 years of age.[116][117][121] The JNC 8 and American College of Physicians recommend the target of 150/90 mmHg for those over 60 years of age,[14][121] but some experts within these groups disagree with this recommendation.[122] Some expert groups have also recommended slightly lower targets in those with diabetes[123] or chronic kidney disease,[124] but others recommend the same target as the general population.[14][118] The issue of what is the best target and whether targets should differ for high-risk individuals is unresolved,[125] although some experts propose more intensive blood pressure lowering than advocated in some guidelines.[126]

The 2025 American Heart Association guidelines recommend medication for all adults with average blood pressure 140/90 mmHg or higher.[127] It also recommends medication for adults with blood pressure 130/80 mmHg or higher with a 10-year risk of cardiovascular disease 7,5% or more, and in those with blood pressure 130/80 mmHg or higher with a 10-year cardiovascular risk of less than 7,5% where blood pressure remains above 130/80 mmHg after 3–6 months of lifestyle modifications.[127]

Lifestyle modifications

[edit]

The first line of treatment for hypertension is lifestyle changes, including dietary changes, physical activity, and weight loss. Though these have all been recommended in scientific advisories,[128] a Cochrane systematic review found no evidence (due to lack of data) for effects of weight loss diets on death, long-term complications or adverse events in persons with hypertension.[129] The review did find a decrease in body weight and blood pressure.[129] Their potential effectiveness is similar to and at times exceeds a single medication.[13] If hypertension is high enough to justify immediate use of medications, lifestyle changes are still recommended in conjunction with medication.

Dietary changes shown to reduce blood pressure include diets with low sodium,[130][131] the DASH diet (Dietary Approaches to Stop Hypertension),[132] which was the best against 11 other diet in an umbrella review,[133] and plant-based diets.[134] A 2024 clinical guideline recommended an increase dietary fiber intake,[135] with a minimum of 28g/day for women and 38g/day for men diagnosed with hypertension.[136]

Increasing dietary potassium has a potential benefit for lowering the risk of hypertension.[137][138] The 2015 Dietary Guidelines Advisory Committee (DGAC) stated that potassium is one of the shortfall nutrients which is under-consumed in the United States.[139] However, people who take certain antihypertensive medications (such as ACE-inhibitors or ARBs) should not take potassium supplements or potassium-enriched salts due to the risk of high levels of potassium.[140]

Physical exercise regimens which are shown to reduce blood pressure include isometric resistance exercise, aerobic exercise, resistance exercise, and device-guided breathing.[141]

A 2020 Cochrane review examined the impact of walking on blood pressure and heart rate in adults. The review found that walking likely reduces systolic blood pressure, with consistent effects across different age groups and both sexes. There was also some evidence that walking may lower diastolic blood pressure and heart rate. Overall, the certainty of evidence ranged from moderate to low, depending on the outcome and subgroup. Walking appears to be a safe, accessible, and potentially effective strategy for supporting cardiovascular health.[142]

Stress reduction techniques such as biofeedback or transcendental meditation may be considered as an add-on to other treatments to reduce hypertension, but do not have evidence for preventing cardiovascular disease on their own.[141][143][144] Self-monitoring and appointment reminders might support the use of other strategies to improve blood pressure control, but need further evaluation.[145]

Medications

[edit]

Several classes of medications, collectively referred to as antihypertensive medications, are available for treating hypertension.

First-line medications for hypertension include thiazide-diuretics, calcium channel blockers, angiotensin converting enzyme inhibitors (ACE inhibitors), and angiotensin receptor blockers (ARBs).[146][14] These medications may be used alone or in combination (ACE inhibitors and ARBs are not recommended for use together); the latter option may serve to minimize counter-regulatory mechanisms that act to restore blood pressure values to pre-treatment levels,[14][147] although the evidence for first-line combination therapy is not strong enough.[148] Most people require more than one medication to control their hypertension.[128] Medications for blood pressure control should be implemented by a stepped care approach when target levels are not reached.[145] Withdrawal of such medications in the elderly can be considered by healthcare professionals, because there is no strong evidence of an effect on mortality, myocardial infarction, or stroke.[149][needs update]

Previously, beta-blockers such as atenolol were thought to have similar beneficial effects when used as first-line therapy for hypertension. However, a Cochrane review that included 13 trials found that the effects of beta-blockers are inferior to those of other antihypertensive medications in preventing cardiovascular disease.[150]

The prescription of antihypertensive medication for children with hypertension has limited evidence. There is limited evidence that compares it with a placebo and shows a modest effect on blood pressure in the short term. Administration of a higher dose did not reduce blood pressure further.[151]

Resistant hypertension

[edit]

Resistant hypertension is defined as high blood pressure that remains above a target level, despite being prescribed three or more antihypertensive drugs simultaneously with different mechanisms of action.[152][13][153] Failing to take prescribed medications as directed is an important cause of resistant hypertension.[154] To confirm true resistant hypertension, the drug treatment regimen should consist of optimal or best tolerated doses. Inadequate blood pressure control should be verified by out-of-office measurement methods, such as home blood pressure monitoring or 24-hour ambulatory blood pressure monitoring, to exclude white-coat effect. Adherence to therapy should be confirmed and secondary causes of hypertension excluded. If these factors are not addressed, the terms pseudoresistant or apparent resistant hypertension are proposed.[13]

Some common secondary causes of resistant hypertension include obstructive sleep apnea, primary aldosteronism and renal artery stenosis, and some rare secondary causes are pheochromocytoma and coarctation of the aorta.[155] As many as one in five people with resistant hypertension have primary aldosteronism, which is a treatable and sometimes curable condition.[156] Resistant hypertension may also result from chronically high activity of the autonomic nervous system, an effect known as neurogenic hypertension.[157] Electrical therapies that stimulate the baroreflex are being studied as an option for lowering blood pressure in people in this situation.[158]

Refractory hypertension is described by one source as elevated blood pressure unmitigated by five or more concurrent antihypertensive agents of different classes.[159] People with refractory hypertension typically have increased sympathetic nervous system activity, and are at high risk for more severe cardiovascular diseases and all-cause mortality.[159][160]

Epidemiology

[edit]
Rates of hypertension in adult men in 2014[161]
Disability-adjusted life year for hypertensive heart disease per 100,000 inhabitants in 2004:[162]

Adults

[edit]

In 2024, one in three or 33% of the world population were estimated to have hypertension.[6] Of all people with hypertension, almost half (about 44%) do not know that they have hypertension.[6] In 1990, about 650 million people had a diagnosis of hypertension, which increased to 1.4 billion by 2024 mostly due a rise of the number of older adults in low- and middle-income countries.[6]

Hypertension is slightly more frequent in men.[9] In people aged under 50 years, more men than women have hypertension,[9] and in ages above 50 years the prevalence of hypertension is the same in men and women.[9] In ages above 65 years, more women than men have hypertension.[13] Hypertension becomes more common with age.[5] Hypertension is common in high, medium, and low-income countries.[2] It is more common in people of low socioeconomic status.[163] Hypertension is around twice as common in diabetics.[164]

In 2019, rates of diagnosed hypertension were highest in Africa (30% for both sexes), and lowest in the Americas (18% for both sexes).[9] Rates also vary markedly within regions with country-level rates as low as 22.8% (men) and 18.4% (women) in Peru and as high as 61.6% (men) and 50.9% (women) in Paraguay.[9]

In 1995, it was estimated that 24% of the United States population had hypertension or were taking antihypertensive medication.[165] By 2004 this had increased to 29%[166][167] and further to 32% (76 million US adults) by 2017.[12] In 2017, with the American guidelines' change in definition for hypertension, 46% of people in the United States are affected.[12] Some data shows African-American adults in the United States have among the highest rates of hypertension in the world at 44%.[168] However, other research argues there has been a "myopic perspective" on American data and notes that other groups, particularly Russians and Eastern Europeans, have markedly higher rates of hypertension than Black Americans.[169] Differences in hypertension rates are multifactorial and under study.[170]

Children

[edit]

Rates of high blood pressure in children and adolescents have increased in the last 20 years in the United States.[171] Childhood hypertension, particularly in pre-adolescents, is more often secondary to an underlying disorder than in adults. Kidney disease is the most common secondary cause of hypertension in children and adolescents. Nevertheless, primary or essential hypertension accounts for most cases.[172]

Prognosis

[edit]
Main article: Complications of hypertension
Diagram illustrating the main complications of persistent high blood pressure

Hypertension is the most important preventable risk factor for premature death worldwide.[173] It increases the risk of ischemic heart disease,[174] stroke,[25] peripheral vascular disease,[175] and other cardiovascular diseases, including heart failure, aortic aneurysms, diffuse atherosclerosis, chronic kidney disease, atrial fibrillation, cancers, leukemia and pulmonary embolism.[11][25] Hypertension is also a risk factor for cognitive impairment and dementia.[25] Other complications include hypertensive retinopathy and hypertensive nephropathy.[30]

History

[edit]
Main article: History of hypertension
Image of veins from Harvey's Exercitatio Anatomica de Motu Cordis et Sanguinis in Animalibus

Measurement

[edit]

Modern understanding of the cardiovascular system began with the work of physician William Harvey (1578–1657), who described the circulation of blood in his book "De motu cordis". The English clergyman Stephen Hales made the first published measurement of blood pressure in 1733.[176][177] However, hypertension as a clinical entity came into its own with the invention of the cuff-based sphygmomanometer by Scipione Riva-Rocci in 1896.[178] This allowed easy measurement of systolic pressure in the clinic. In 1905, Nikolai Korotkoff improved the technique by describing the Korotkoff sounds that are heard when the artery is auscultated with a stethoscope while the sphygmomanometer cuff is deflated.[177] This permitted systolic and diastolic pressure to be measured.

Identification

[edit]

Symptoms similar to those of patients with a hypertensive crisis are discussed in medieval Persian medical texts in the chapter of "fullness disease".[179] The symptoms include headache, heaviness in the head, sluggish movements, general redness and warm to touch feel of the body, prominent, distended and tense vessels, a fullness of the pulse, distension of the skin, coloured and dense urine, loss of appetite, weak eyesight, impairment of thinking, yawning, drowsiness, vascular rupture, and hemorrhagic stroke.[180] Fullness disease was presumed to be due to an excessive amount of blood within the blood vessels.

Descriptions of hypertension as a disease came, among others, from Thomas Young in 1808 and especially Richard Bright in 1836.[176] The first report of elevated blood pressure in a person without evidence of kidney disease was made by Frederick Akbar Mahomed (1849–1884).[181]

Until the 1990s, systolic hypertension was defined as systolic blood pressure of 160 mmHg or greater.[182] In 1993, the WHO/ISH guidelines defined 140 mmHg as the threshold for hypertension.[183]

Treatment

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Historically, the treatment for what was called the "hard pulse disease" consisted of reducing the quantity of blood by bloodletting or the application of leeches.[176] This was advocated by The Yellow Emperor of China, Cornelius Celsus, Galen, and Hippocrates.[176] The therapeutic approach for the treatment of hard pulse disease included lifestyle changes (staying away from anger and sexual intercourse) and dietary program for patients (avoiding the consumption of wine, meat, and pastries, reducing the volume of food in a meal, maintaining a low-energy diet and the dietary usage of spinach and vinegar).

In the 19th and 20th centuries, before effective pharmacological treatment for hypertension became possible, three treatment modalities were used, all with numerous side effects: strict sodium restriction (for example the rice diet[176]), sympathectomy (surgical ablation of parts of the sympathetic nervous system), and pyrogen therapy (injection of substances that caused a fever, indirectly reducing blood pressure).[176][184]

The first chemical for hypertension, sodium thiocyanate, was used in 1900 but had many side effects and was unpopular.[176] Several other agents were developed after the Second World War, the most popular and reasonably effective of which were tetramethylammonium chloride, hexamethonium, hydralazine, and reserpine (derived from the medicinal plant Rauvolfia serpentina). None of these were well tolerated.[185][186] A major breakthrough was achieved with the discovery of the first well-tolerated orally available agents. The first was chlorothiazide, the first thiazide diuretic and developed from the antibiotic sulfanilamide, which became available in 1958.[176][187] Subsequently, beta blockers, calcium channel blockers, angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers, and renin inhibitors were developed as antihypertensive agents.[184]

Society and culture

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Awareness

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Graph showing the prevalence of awareness, treatment, and control of hypertension compared between the four studies of NHANES[166]

The World Health Organization has identified hypertension (high blood pressure) as the leading cause of cardiovascular mortality.[188] The World Hypertension League (WHL), an umbrella organization of 85 national hypertension societies and leagues, recognized that more than 50% of the hypertensive population worldwide are unaware of their condition.[188] To address this problem, the WHL initiated a global awareness campaign on hypertension in 2005 and dedicated 17 May of each year as World Hypertension Day.[189]

Economics

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High blood pressure is the most common chronic medical problem prompting visits to primary health care providers in the US. The American Heart Association estimated the direct and indirect costs of high blood pressure in 2010 as $76.6 billion.[168] In the US, 80% of people with hypertension are aware of their condition, 71% take some antihypertensive medication, but only 48% of people aware that they have hypertension adequately control it.[168] Adequate management of hypertension can be hampered by inadequacies in the diagnosis, treatment, or control of high blood pressure.[190] Health care providers face many obstacles to achieving blood pressure control, including resistance to taking multiple medications to reach blood pressure goals. People also face the challenges of adhering to medical schedules and making lifestyle changes. Nonetheless, the achievement of blood pressure goals is possible, and most importantly, lowering blood pressure significantly reduces the risk of death due to heart disease and stroke, the development of other debilitating conditions, and the cost associated with advanced medical care.[191][192] The cost of medications discourages many patients from continuing treatment.[193]

Other animals

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Hypertension in cats is indicated by a systolic blood pressure greater than 150 mmHg, with amlodipine the usual first-line treatment. A cat with a systolic blood pressure above 170 mmHg is considered hypertensive. If a cat has other problems, such as kidney disease or retina detachment, then a blood pressure below 160 mmHg may also need to be monitored.[194]

Normal blood pressure in dogs can differ substantially between breeds, but hypertension is often diagnosed if systolic blood pressure is above 160 mmHg, particularly if this is associated with target organ damage.[195] Inhibitors of the renin-angiotensin system and calcium channel blockers are often used to treat hypertension in dogs, although other drugs may be indicated for specific conditions causing high blood pressure.[195]

See also

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References

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Further reading

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Hypertension

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from Grokipedia
Hypertension, commonly known as high , is a chronic medical condition characterized by persistently elevated pressure in the arteries, which forces the heart to work harder to pump blood throughout the body. It is typically defined as a systolic of 130 mm Hg or higher, or a diastolic of 80 mm Hg or higher, based on the 2025 guidelines from major health organizations such as the and the ; however, some international standards, like those from the , use a threshold of 140/90 mm Hg or higher. This condition affects the cardiovascular system primarily but can lead to widespread organ damage if uncontrolled. Globally, hypertension affects 1 in 3 adults (approximately 1.3 billion people as of 2019 data), with more than three-quarters of adults with hypertension residing in low- and middle-income countries (LMICs). Awareness is low, with nearly half unaware globally, and control rates in LMICs are poor (around 10% in some studies). Hypertension is known as the "silent killer" because it is often asymptomatic until severe complications occur. The WHO's 2023 open access global report on hypertension emphasizes that effective treatment could prevent millions of deaths, strokes, and heart attacks between 2023 and 2050. In the United States, nearly half of all adults—about 120 million people—have hypertension, though many remain unaware or untreated, contributing to its status as a major challenge. The condition is classified into two main types: primary (, which accounts for about 90–95% of cases and develops gradually without a specific identifiable cause, often linked to genetic and environmental factors; and , which arises suddenly from underlying conditions such as , disorders, or certain medications. Key risk factors for hypertension include non-modifiable elements like advancing age (prevalence rises to over 70% in those aged 60 and older), family history, and race (higher rates among individuals), as well as modifiable factors such as , physical inactivity, high sodium intake, excessive alcohol consumption, use, and . Pathophysiologically, it involves mechanisms like increased peripheral , overactivation of the renin-angiotensin-aldosterone , and heightened sympathetic nervous activity, which elevate arterial pressure over time. Most individuals experience no symptoms, earning it the moniker "silent killer," but severe or prolonged cases may present with headaches, , nosebleeds, or . Untreated hypertension significantly increases the risk of serious complications, including heart attack, , heart failure, kidney damage, , vision loss, and cognitive impairments like . involves repeated measurements, often confirmed on separate occasions, with classifications ranging from elevated (120–129/<80 mm Hg) to stage 2 hypertension (≥140/≥90 mm Hg) or hypertensive crisis (>180/>120 mm Hg, requiring immediate medical attention). Management focuses on lifestyle modifications—such as adopting a low-sodium , engaging in at least 150 minutes of moderate weekly, maintaining a healthy weight, and quitting —combined with medications like diuretics, inhibitors, or beta-blockers for those needing pharmacological intervention. Effective control can reduce cardiovascular risks by up to 30–40%, underscoring the importance of regular screening and early intervention.

Signs and Symptoms

General Manifestations

Hypertension is frequently , earning it the moniker "silent killer" due to its ability to progress undetected while causing progressive damage to blood vessels and organs. Most individuals experience no noticeable signs, even when reaches dangerously elevated levels, which underscores the importance of routine screening. Globally, nearly half of people with hypertension remain unaware of their condition, contributing to higher risks of complications like . In mild cases, hypertension may occasionally manifest with nonspecific symptoms such as headaches, , or , though these are uncommon and not reliably indicative of the condition. Headaches, for instance, can arise from vascular strain but are more typical in advanced stages rather than early hypertension. has been reported in a substantial proportion of affected individuals, potentially linked to reduced cardiac or associated comorbidities. These subtle presentations often go unnoticed, delaying until routine evaluations reveal elevated . Physical examination can uncover indirect signs of hypertension, particularly through targeted assessments of end organs. Fundoscopic examination of the may reveal arteriolar narrowing, arteriovenous (AV) nicking, and flame-shaped hemorrhages, reflecting chronic vascular stress in the eyes. Cardiac might detect signs of (LVH), such as an accentuated second heart sound or a displaced , resulting from the heart's adaptation to increased over time. Additionally, over the could identify renal artery bruits, which suggest underlying secondary causes like . These manifestations, though subtle, signal early end-organ damage from sustained high pressure: retinal changes indicate microvascular injury akin to broader vascular , LVH represents cardiac remodeling that heightens arrhythmia risk, and renal bruits point to potential renovascular compromise. Such findings during routine exams highlight hypertension's insidious progression, where asymptomatic elevation quietly erodes organ function before overt symptoms emerge.

Hypertensive Crisis

A hypertensive crisis is defined as a severe elevation in , typically with systolic blood pressure exceeding 180 mm Hg or diastolic blood pressure exceeding 120 mm Hg. This condition is categorized into two types: , which involve acute end-organ damage such as , , acute , , or , and hypertensive urgencies, characterized by severe blood pressure elevation without evidence of acute target organ damage. Symptoms of a often include severe , visual disturbances, , dyspnea, and , signaling potential acute organ involvement. requires prompt evaluation to assess for end-organ damage, including electrocardiogram (ECG) to detect cardiac ischemia or arrhythmias, laboratory tests such as levels for myocardial injury and for renal function, and imaging like computed tomography (CT) of the head for neurological complications or chest for pulmonary or cardiac issues. Initial management of hypertensive emergencies focuses on gradual blood pressure reduction to prevent further organ damage, aiming to lower mean arterial pressure by approximately 25% within the first hour, followed by further cautious normalization; full treatment details are addressed in dedicated management sections. Untreated hypertensive crises carry a high mortality risk, with 1-year survival rates below 21% in historical untreated cases. The incidence of hypertensive crisis affects approximately 1-2% of patients with hypertension annually.

In Pregnancy

Hypertensive disorders of pregnancy encompass a spectrum of conditions characterized by new-onset hypertension after 20 weeks of gestation, including , , and . is defined as systolic of 140 mm Hg or higher, or diastolic of 90 mm Hg or higher, on two occasions at least 4 hours apart, without or other features of . involves the same criteria accompanied by (typically ≥300 mg in a 24-hour collection) or evidence of end-organ dysfunction, such as , renal insufficiency, impaired liver function, , or cerebral/visual symptoms. represents a severe progression of marked by new-onset generalized tonic-clonic seizures not attributable to other causes. These disorders collectively affect 5-10% of pregnancies worldwide, with comprising the majority and occurring in approximately 3-5%. Symptoms of these conditions often overlap with normal pregnancy changes but can signal progression to severe disease. Common manifestations include edema (particularly in the face and hands), sudden weight gain, persistent headache, visual disturbances (such as blurred vision or scotoma), and epigastric or right upper quadrant pain due to hepatic involvement. Proteinuria may be asymptomatic but indicates renal involvement. Maternal risks escalate with preeclampsia and eclampsia, including placental abruption, stroke, disseminated intravascular coagulation, and HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count), which complicates 10-20% of severe preeclampsia cases. Fetal implications involve intrauterine growth restriction, preterm birth (often iatrogenic to protect maternal health), and increased perinatal mortality, with risks amplified in superimposed preeclampsia on preexisting chronic hypertension. Diagnosis requires careful timing relative to and exclusion of chronic hypertension. measurements should use validated devices, with confirmation on separate occasions; or home monitoring can aid accuracy but is not always feasible in . For , beyond hypertension, assessment includes a spot protein-to- ≥0.3 mg/mg (equivalent to ≥300 mg/24 hours) or, in its absence, laboratory evidence of organ involvement such as serum >1.1 mg/dL or doubling of baseline, platelet count <100,000/μL, or liver transaminases twice the upper limit of normal. Eclampsia is diagnosed clinically by seizures in the context of , prompting immediate magnesium sulfate administration. The 2024 European Society of Cardiology guidelines emphasize low-dose aspirin (75-150 mg daily) prophylaxis starting at 12 weeks gestation until 36 weeks or delivery for high-risk women (e.g., history of , multiple gestation, or chronic hypertension) to reduce incidence by 10-20%. Delivery remains the definitive treatment, timed based on severity and .

In Children and Adolescents

Hypertension in children and adolescents is defined as systolic or diastolic blood pressure at or above the 95th percentile for age, sex, and height on three or more separate occasions, according to guidelines from the American Academy of Pediatrics (AAP) and endorsed by the American Heart Association (AHA). These percentiles account for normal variations in blood pressure related to growth and development, with updated tools available in 2025 for precise calculation via age-, sex-, and height-adjusted models. The global prevalence of sustained hypertension in this population is approximately 3.89%, with rates increasing to over 10% when including elevated blood pressure, particularly among those with obesity or overweight. Unlike in adults, symptoms are often absent or subtle due to the greater elasticity of pediatric blood vessels, which may buffer against immediate end-organ damage. In children and adolescents, hypertension is predominantly secondary, accounting for up to 80-90% of cases, with renal parenchymal disease as the most common underlying cause, followed by cardiac conditions such as coarctation of the aorta. Other renal etiologies include chronic kidney disease and renovascular hypertension, while cardiac issues often involve structural abnormalities leading to increased afterload. Primary hypertension, linked to lifestyle factors like obesity, is rising but remains less frequent than in adults. Most affected youth remain asymptomatic, but when present, manifestations may include headaches, fatigue, and poor sleep quality; in severe or longstanding cases, growth failure can occur due to associated metabolic or renal disturbances. Hypertensive emergencies, though rare, can present with seizures, vomiting, or encephalopathy, particularly in infants who may show irritability or apnea. White coat hypertension, where clinic readings are elevated due to anxiety but ambulatory monitoring is normal, is common, affecting up to 43% of referred children and often requiring confirmation with out-of-office measurements. Physical examination may reveal bounding pulses, suggestive of hyperdynamic circulation in conditions like renal artery stenosis or anemia-associated hypertension, and organomegaly such as hepatosplenomegaly in cases of chronic renal disease. Left ventricular hypertrophy or retinal changes may also indicate target-organ involvement, underscoring the need for early screening in at-risk groups like obese adolescents.

Causes

Primary Hypertension

Primary hypertension, also known as essential hypertension, accounts for 90-95% of all hypertension cases and is defined as persistently elevated blood pressure without an identifiable secondary cause. This form arises from complex interactions between genetic predisposition and environmental influences, leading to a gradual increase in blood pressure over many years. Unlike secondary hypertension, which stems from specific underlying conditions, primary hypertension has no single causative factor but rather multifactorial origins that contribute to its idiopathic nature. Key risk factors for primary hypertension include genetic factors, with heritability estimates for blood pressure ranging from 30% to 50%, indicating a substantial inherited component. Advancing age is a major contributor, as arterial stiffness increases and vascular function declines over time. Other modifiable risks encompass obesity, which promotes endothelial dysfunction and inflammation; salt sensitivity, where high dietary sodium intake exacerbates blood pressure elevation in susceptible individuals; sedentary lifestyle, leading to reduced cardiovascular fitness; and excessive alcohol consumption, which can directly raise blood pressure through vascular and neurohormonal effects. These factors often interact synergistically to heighten risk. Among the pathogenic mechanisms, increased peripheral vascular resistance plays a central role, driven by structural changes such as arteriolar wall thickening and reduced lumen diameter in resistance vessels. contributes by impairing vasodilation and promoting sodium retention, while sympathetic nervous system overactivity heightens vasoconstriction and cardiac output. These processes are interconnected and detailed further in pathophysiology discussions. Emerging research highlights the polygenic basis of primary hypertension, with no single gene dominating but rather thousands of common variants contributing small effects. Genome-wide association studies (GWAS) since 2020 have identified numerous loci influencing blood pressure traits, enabling the development of polygenic risk scores that predict hypertension susceptibility and cardiovascular outcomes with improving accuracy across diverse populations.

Secondary Hypertension

Secondary hypertension refers to elevated blood pressure resulting from an identifiable underlying medical condition, accounting for approximately 5% to 10% of all hypertension cases in adults. Unlike primary hypertension, secondary forms often present opportunities for cure or significant improvement through targeted treatment of the root cause, underscoring the importance of screening in select patients. Recent studies, including large cohort analyses, suggest this prevalence may be underestimated, particularly in resistant hypertension where rates can exceed 20%. The most frequent causes fall into renal, endocrine, vascular, sleep-related, and medication-induced categories. Renal disorders, such as chronic kidney disease and renovascular stenosis due to atherosclerotic or fibromuscular dysplasia, contribute to about 2% to 5% of secondary hypertension cases, with renovascular stenosis specifically implicated in roughly 1% to 5% of overall hypertension. Endocrine etiologies include primary aldosteronism (Conn's syndrome), which affects 5% to 14% of hypertensive patients and up to 20-30% of those with resistant hypertension according to 2025 Endocrine Society guidelines and cohort studies; Cushing's syndrome and pheochromocytoma are rarer, each accounting for less than 1%. Other notable causes encompass coarctation of the aorta (prevalent in 0.03% to 0.1% of the general population but a key reversible factor in young adults), obstructive sleep apnea (linked to 20% to 40% of resistant cases in obese individuals), and drug-induced hypertension from agents like nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or oral contraceptives. Clinical clues prompting evaluation for secondary hypertension include onset before age 30 or after 55, resistant blood pressure despite three antihypertensive medications, severe hypertension exceeding 180/110 mmHg, and biochemical abnormalities such as hypokalemia (occurring in approximately 20-40% of primary aldosteronism cases), which increases suspicion for primary aldosteronism as it is found in up to 30% of hypertensive patients with hypokalemia. Additional red flags are an abdominal bruit indicating renovascular disease or episodic symptoms like headaches and palpitations hinting at pheochromocytoma. Diagnostic screening often begins with targeted tests: the plasma aldosterone-to-renin ratio (ARR) for endocrine causes, where a ratio greater than 20 to 30 with elevated aldosterone prompts confirmatory saline infusion or fludrocortisone suppression; renal artery imaging via duplex ultrasound or CT angiography for renovascular suspicion; polysomnography for sleep apnea; and echocardiography or MRI for coarctation. A thorough medication review is essential for drug-related cases. Addressing the underlying condition can resolve hypertension in many instances, such as surgical correction of coarctation yielding normalization in approximately 50-70% of patients or adrenalectomy for unilateral primary aldosteronism curing hypertension in 30% to 60% of cases and improving control in most others. Revascularization for renal artery stenosis or continuous positive airway pressure for sleep apnea similarly enhances blood pressure management, reducing reliance on medications and mitigating cardiovascular risks. Early identification through systematic screening in high-risk groups is thus critical to leverage these reversible pathways.

Pathophysiology

Hemodynamic and Vascular Mechanisms

Hypertension arises from alterations in the fundamental hemodynamic determinants of blood pressure, primarily governed by the equation for mean arterial pressure (MAP), which is derived from the steady-state relationship between blood flow and vascular resistance. MAP is calculated as the product of cardiac output (CO) and total peripheral resistance (TPR): MAP=CO×TPR\text{MAP} = \text{CO} \times \text{TPR} This equation stems from the principle that arterial pressure represents the force exerted by blood volume flow (CO) against the resistance offered by the systemic vasculature (TPR), assuming a closed circulatory system in equilibrium. In essential hypertension, the primary driver of elevated MAP is an increase in TPR, often through vasoconstriction of arterioles and reduced arterial compliance, while CO remains normal or near-normal in the early stages. Systemic vascular resistance increases due to heightened vascular tone and structural changes in the vessel walls, leading to persistent vasoconstriction that elevates TPR without initially affecting CO. As hypertension progresses, particularly in cases involving volume overload such as obesity-related hypertension, CO may rise to accommodate expanded plasma volume, further contributing to elevated MAP. Endothelial dysfunction plays a central role in these vascular changes, characterized by diminished production of nitric oxide (NO), a key vasodilator, which impairs endothelium-dependent relaxation and promotes vasoconstriction. Concurrently, increased endothelin-1 expression, a potent vasoconstrictor, exacerbates this imbalance, fostering a pro-hypertensive state in the vascular endothelium. Arterial stiffness, another critical vascular mechanism, results from age-related and hypertensive remodeling, including excessive collagen deposition in the arterial media and adventitia, which reduces vessel distensibility and compliance. This stiffening disproportionately affects large elastic arteries like the aorta, leading to a widened pulse pressure—the difference between systolic and diastolic pressures—as systolic pressure rises while diastolic pressure falls due to faster pressure wave propagation and reduced damping. With advancing age, this widening of pulse pressure becomes more pronounced, reflecting progressive large-artery stiffening and amplifying the hemodynamic burden on the cardiovascular system, which can contribute to end-organ damage such as left ventricular hypertrophy.

Neurohormonal and Renal Factors

The renin-angiotensin-aldosterone system (RAAS) plays a central role in the neurohormonal regulation of blood pressure, particularly in , by modulating vascular tone and fluid balance. Renin, an enzyme secreted by the juxtaglomerular cells of the kidney in response to reduced renal perfusion pressure, low sodium delivery to the distal tubule, or sympathetic stimulation, cleaves angiotensinogen (produced by the liver) to form angiotensin I. (ACE), primarily in the lungs, then converts angiotensin I to angiotensin II, a potent vasoconstrictor that elevates blood pressure by increasing systemic vascular resistance and promoting release from the adrenal cortex. Aldosterone enhances sodium reabsorption in the renal collecting ducts, leading to water retention and expanded plasma volume, which further sustains hypertension. This cascade can be summarized as: low renal perfusion → renin release → angiotensin II formation → vasoconstriction and aldosterone-mediated sodium retention → elevated blood pressure. Overactivity of the sympathetic nervous system contributes to hypertension by augmenting RAAS activation and directly influencing vascular and renal function. Increased sympathetic outflow, often originating from central nervous system dysregulation, stimulates renin release via β1-adrenergic receptors in the kidney and promotes norepinephrine-mediated vasoconstriction, leading to sustained elevations in blood pressure. This overactivity is evident in essential hypertension, where muscle sympathetic nerve activity is heightened, correlating with disease severity and resistance to treatment. Additionally, an imbalance in natriuretic peptides, such as atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), exacerbates this process; these peptides normally counteract RAAS by promoting natriuresis, vasodilation, and inhibition of renin and aldosterone secretion, but their reduced levels or impaired signaling in hypertension diminish this protective effect, allowing unchecked sodium retention and pressure elevation. Renal mechanisms are integral to neurohormonal hypertension, primarily through alterations in pressure natriuresis and sodium handling. Pressure natriuresis refers to the kidney's ability to increase sodium and water excretion in response to elevated renal perfusion pressure, thereby normalizing blood volume; in hypertension, this curve shifts rightward due to intrinsic renal defects or neurohormonal influences, requiring higher pressures to achieve adequate natriuresis and perpetuating sodium retention. Defects in renal sodium handling, such as impaired proximal tubule reabsorption or distal tubule dysfunction influenced by RAAS overactivation, further impair this process, leading to volume-dependent hypertension. RAAS inhibitors, including ACE inhibitors and angiotensin receptor blockers, effectively target these pathways, reducing blood pressure in a majority of patients by blocking angiotensin II effects and restoring natriuretic balance. Recent research highlights emerging influences, such as gut microbiome alterations modulating RAAS activity through microbial metabolites that affect angiotensin II signaling, potentially offering new therapeutic avenues. Advances in 2025 include small interfering RNA (siRNA) therapies targeting RAAS components, such as zilebesiran, which silences hepatic angiotensinogen expression to suppress the entire cascade at its source, demonstrating sustained blood pressure reductions in clinical trials with quarterly dosing. These therapies address limitations of traditional RAAS inhibitors by providing longer-lasting effects and improved adherence, particularly in resistant hypertension.

Diagnosis

Blood Pressure Measurement Techniques

Blood pressure measurement in clinical settings primarily relies on office-based techniques using either auscultatory or oscillometric methods to assess hypertension accurately. The auscultatory method involves a mercury or aneroid sphygmomanometer and stethoscope to detect Korotkoff sounds over the brachial artery, requiring trained personnel for precise detection of systolic and diastolic phases, though it is susceptible to observer errors such as rapid cuff deflation exceeding 2-3 mmHg per second. In contrast, the oscillometric method, commonly used in automated devices, detects arterial pulsations through cuff pressure oscillations and is preferred for its reduced operator dependence when the device is validated, making it suitable for both attended and unattended measurements. Accurate office measurements necessitate standardized protocols to minimize variability. Proper cuff selection is essential, with the bladder width covering 40% of arm circumference and length encircling 80% to avoid overestimation by up to 20 mmHg from an undersized cuff or underestimation from an oversized one; validated devices are recommended, and resources like the Validate BP list ensure compliance. Patients should be seated with back supported, feet flat, and arm at heart level after 5 minutes of rest, avoiding caffeine, exercise, or talking prior to measurement to prevent artifacts. A single reading is insufficient for diagnosis, as it can lead to misclassification; instead, the average of at least two readings, taken 1-2 minutes apart, over two or more visits is required, with improper techniques potentially causing errors of 10-20 mmHg. Out-of-office monitoring complements office assessments, particularly ambulatory blood pressure monitoring (ABPM) and home blood pressure monitoring (HBPM), to detect phenomena like white-coat or masked hypertension. ABPM employs a portable oscillometric device for 24-hour automated recordings, typically at 15-30 minute intervals daytime and 30-60 minutes nighttime, providing averages such as daytime ≥130/80 mmHg corresponding to elevated risk, and is a Class I recommendation for confirming diagnoses, including stage 1 hypertension (office 130-139/80-89 mmHg) in the 2025 guidelines. HBPM involves self-measurements with validated upper-arm cuff devices over several days, averaging ≥130/80 mmHg to align with office thresholds, and is emphasized for ongoing management, especially when integrated with telehealth or team-based care to improve control. These methods enhance prognostic accuracy over office readings alone, with ABPM particularly valued for its ability to predict cardiovascular events independently.

Additional Diagnostic Tests

Following confirmation of hypertension through standardized blood pressure measurement techniques, additional diagnostic tests are essential to identify underlying causes, assess target organ damage, and evaluate cardiovascular risk. These evaluations help guide treatment decisions and monitor complications such as chronic kidney disease (CKD) and left ventricular hypertrophy (LVH). Laboratory assessments form the cornerstone of this evaluation, including a complete blood count, basic metabolic panel with electrolytes (sodium, potassium, and calcium), thyroid-stimulating hormone (TSH), serum creatinine to calculate estimated glomerular filtration rate (eGFR), fasting glucose or hemoglobin A1c, lipid profile, and urinalysis with urine albumin-to-creatinine ratio (UACR). Abnormal electrolytes may indicate secondary hypertension due to conditions like hyperaldosteronism, while an eGFR below 60 mL/min/1.73 m² signals CKD risk, warranting closer monitoring and specific therapies. The lipid profile and fasting glucose contribute to overall cardiovascular disease (CVD) risk stratification, with tests repeated annually or as needed based on initial results. For suspected secondary causes, the plasma aldosterone-to-renin activity ratio is recommended as a screening tool for primary aldosteronism, particularly in patients with resistant hypertension or hypokalemia. Urinalysis detects proteinuria, and a UACR of 30 mg/g or higher identifies early kidney damage, influencing the choice of renin-angiotensin system inhibitors. Cardiac evaluations include a 12-lead electrocardiogram (ECG) to detect LVH, a common marker of prolonged hypertension exposure, and echocardiography to assess left ventricular structure and function. Echocardiography provides detailed insights into systolic and diastolic dysfunction, refining CVD risk estimates beyond basic labs. These tests are performed at diagnosis, especially in patients with symptoms or risk factors for heart disease. Renal imaging, such as ultrasound or Doppler studies, is indicated to evaluate for renal artery stenosis in cases of resistant hypertension or asymmetric kidney sizes. This non-invasive approach helps identify structural abnormalities contributing to secondary hypertension without routine use in all patients. Routine screening for target organ damage integrates these tests, emphasizing eGFR and UACR for renal involvement, ECG and echocardiography for cardiac effects, and fundoscopy for retinopathy when appropriate. Early detection of damage, such as reduced eGFR, informs aggressive management to prevent progression. Integration of the 2025 PREVENT risk calculator enhances CVD assessment by incorporating lab results like lipids and glucose, along with demographics and comorbidities, to estimate 10-year risk; a threshold of 7.5% or higher supports intensified therapy. This tool, updated for broader applicability, is used at diagnosis to personalize prevention strategies.

Classification in Adults

Hypertension in adults is classified based on office blood pressure measurements, with categories defined by systolic and diastolic thresholds in millimeters of mercury (mmHg). These classifications guide risk assessment and management decisions according to the 2025 / guideline. The categories emphasize the importance of consistent readings obtained through validated techniques to ensure accuracy. The following table outlines the blood pressure categories for adults:
CategorySystolic BP (mmHg)Diastolic BP (mmHg)
Normal<120<80
Elevated120–129<80
Stage 1 Hypertension130–139or 80–89
Stage 2 Hypertension≥140or ≥90
Hypertensive Crisis>180and/or >120
A blood pressure reading of 150/100 mmHg, commonly referred to as "15 por 10" or "15 by 10" in some Portuguese-speaking regions, is classified as stage 2 hypertension. This indicates significantly elevated arterial pressure, increasing risks for heart disease, stroke, kidney damage, and other complications if unmanaged. Individuals with such readings should consult a physician immediately for evaluation and diagnosis. Recommended lifestyle changes include reducing salt intake, engaging in regular physical activity (such as 150 minutes of moderate exercise weekly), maintaining a healthy weight, limiting alcohol consumption, quitting smoking, and managing stress. Medication may be prescribed as needed. If severe symptoms such as chest pain, severe headache, vision changes, or shortness of breath occur, seek emergency medical care. This staging system, unchanged in thresholds from prior guidelines but integrated with updated risk tools, identifies individuals requiring intervention. Hypertensive crisis warrants immediate medical evaluation due to potential acute organ damage. Treatment thresholds for stage 1 hypertension incorporate 10-year (CVD) risk assessment using the PREVENT equations, a refinement over previous pooled cohort equations. For adults with stage 1 hypertension and a PREVENT-estimated 10-year CVD risk of ≥7.5%, pharmacologic is recommended immediately alongside modifications if systolic BP is ≥130 mmHg. In those with lower risk (<7.5%), interventions are initiated first, with medication added after 3–6 months if BP remains ≥130/80 mmHg. This risk-based approach aims to personalize care and optimize outcomes. Isolated systolic hypertension, characterized by elevated systolic BP (≥130 mmHg) with normal diastolic BP (<80 mmHg), is particularly common in older adults due to age-related arterial stiffening. The guideline prioritizes systolic targets without emphasizing diastolic elevation, recommending a goal of <130 mmHg systolic BP for those at increased CVD risk, with efforts to achieve <120 mmHg if tolerated based on individual factors like comorbidities and tolerance.

Classification in Children

The classification of hypertension in children and adolescents relies on age-, sex-, and height-specific s derived from normative data from the 2017 American Academy of Pediatrics (AAP) guideline, rather than fixed absolute thresholds used in adults. This approach accounts for physiological variations during growth. Normal blood pressure is defined as below the 90th . Elevated blood pressure is >=90th but <95th , or 120 to 129/<80 mmHg (whichever is lower) for those >=13 years. Stage 1 hypertension is >=95th but <95th + 12 mmHg, or 130 to 139/80 to 89 mmHg (whichever is lower). Stage 2 hypertension is >=95th + 12 mmHg, or >=140/90 mmHg (whichever is lower). These categories require confirmation on at least three separate occasions to distinguish persistent hypertension from transient elevations. In pediatric populations, hypertension is predominantly secondary, particularly in younger children, with underlying causes such as renal or cardiovascular disorders accounting for 45% to 85% of cases in specialized clinics. This contrasts with the increasing prevalence of primary hypertension linked to in adolescents. Accurate classification is crucial, as untreated pediatric hypertension can lead to long-term cardiovascular risks. Additionally, the effect—where anxiety in clinical settings elevates readings—is more prevalent in children than adults, often affecting up to 52% of referred cases, necessitating or monitoring for confirmation. Recent reviews as of have addressed limitations in traditional norms by discussing obesity-adjusted references, recognizing that standard tables may underestimate hypertension in obese youth due to exclusion of overweight children in normative data. These discussions highlight ongoing knowledge gaps in inclusive normative data, but the core classification remains based on the 2017 AAP guideline.

Prevention

Lifestyle Modifications for Prevention

Lifestyle modifications represent a of primary prevention for hypertension, particularly in at-risk populations such as those with prehypertension, , or family history of the condition. These evidence-based strategies target modifiable risk factors to lower and reduce the incidence of hypertension without pharmacological intervention. Comprehensive adoption of multiple changes, including dietary adjustments, , and behavioral shifts, has demonstrated substantial benefits in large-scale clinical trials. The Dietary Approaches to Stop Hypertension (DASH) eating plan is a key dietary intervention emphasizing high intake of fruits, vegetables, whole grains, and low-fat dairy while limiting saturated fats, sweets, and sodium to less than 2,300 mg per day. This pattern promotes nutrient-rich foods that support vascular health and electrolyte balance, leading to systolic blood pressure reductions of approximately 5-11 mmHg in individuals with elevated blood pressure. Clinical trials have shown that even without sodium restriction, the DASH diet lowers blood pressure within weeks compared to a typical American diet. Weight management through caloric restriction and balanced is another critical modification, with evidence indicating that a 5-10% reduction in body weight, particularly when accompanied by reductions in waist circumference or central adiposity, can decrease systolic by 5-20 mmHg in adults. This effect is attributed to decreased activity and improved insulin sensitivity, which help prevent the progression to hypertension. Sustained modest has been linked to a 20-30% lower risk of developing hypertension over several years. Regular , recommended at a minimum of 150 minutes per week of moderate-intensity activity such as brisk walking or , enhances and endothelial function, reducing systolic by 4-9 mmHg. Guidelines from major health organizations endorse this level of activity for all adults to mitigate hypertension risk, with benefits accruing from consistent participation that also aids in weight control. Moderating alcohol consumption is advised, with limits of no more than two standard drinks per day for men and one for women, as excessive intake raises through mechanisms like increased and vascular stiffness. Adhering to these thresholds can prevent alcohol-related elevations in and lower hypertension risk by up to 20% in moderate drinkers. Smoking cessation is essential, as tobacco use accelerates vascular damage and sympathetic activation, contributing to hypertension development; quitting reduces this risk by improving arterial compliance and decreasing the incidence of hypertension by 25-50% within years of . Support programs combining counseling and facilitate long-term success and yield cardiovascular protective effects. Stress management techniques, including mindfulness-based practices, , and , help counteract chronic stress-induced elevations by modulating the . Regular implementation of these methods can lower systolic by 2-5 mmHg and support overall prevention efforts in high-stress individuals. Combined lifestyle modifications amplify preventive outcomes, with trials like the PREMIER study demonstrating that integrated interventions—encompassing , , exercise, and sodium reduction—reduce by 6-12 mmHg and lower hypertension incidence by 20-50% over 18-48 months compared to usual care. Similarly, the Trials of Hypertension Prevention II (TOHP II) showed that combined with sodium restriction decreased hypertension development by 38% during extended follow-up. These multifaceted approaches not only prevent hypertension but also enhance overall cardiovascular health. Emerging emphases in 2025 highlight precision nutrition, leveraging genomic profiling to tailor dietary recommendations for hypertension prevention, such as personalized sodium or intake based on gene-diet interactions. This approach promises to optimize outcomes in genetically susceptible individuals by addressing variability in metabolic responses to standard advice.

Pharmacological Prevention in High-Risk Groups

Pharmacological prevention of hypertension targets individuals at elevated risk for cardiovascular disease (CVD), particularly those with high-normal blood pressure (defined as stage 1 hypertension: 130-139 mm Hg systolic or 80-89 mm Hg diastolic) accompanied by comorbidities such as diabetes mellitus or chronic kidney disease (CKD). In these groups, early initiation of low-dose antihypertensive therapy aims to delay or prevent the onset of frank hypertension and mitigate associated organ damage, with evidence supporting a focus on renin-angiotensin system (RAS) inhibitors. The 2025 American Heart Association/American College of Cardiology (AHA/ACC) guideline incorporates the PREVENT (Precision Risk Estimation to inform Treatment) equation to estimate 10-year CVD risk, recommending pharmacologic intervention alongside lifestyle modifications for adults with stage 1 hypertension and a PREVENT risk of ≥7.5%, with a higher threshold of ≥10% for those with diabetes or target organ damage. This threshold identifies those likely to benefit from early drug therapy to avert progression to stage 2 hypertension (≥140/90 mm Hg) and subsequent CVD events. In patients with diabetes and high-normal blood pressure, low-dose angiotensin-converting enzyme () inhibitors or angiotensin II receptor blockers (ARBs) are preferred due to their dual benefits in blood pressure control and renoprotection. For instance, these agents reduce the progression from microalbuminuria to macroalbuminuria—a precursor to overt nephropathy and hypertension—by approximately 30-50% in normotensive or prehypertensive individuals with . Similarly, in those with CKD and but without established hypertension, inhibitors or ARBs slow disease progression and lower the risk of end-stage renal disease by about 31%, thereby delaying hypertension development linked to worsening kidney function. The TROPHY trial demonstrated that low-dose candesartan (an ARB) in prehypertensive adults reduced the incidence of new-onset hypertension by 66% during two years of active treatment, with a sustained 16% over four years including post-treatment follow-up. For broader CVD prevention in high-risk stage 1 hypertension per PREVENT criteria (≥7.5% risk), statins may be initiated concurrently with antihypertensives to address and further lower overall cardiovascular burden, as elevated amplifies hypertension-related risks. This combined approach, integrated with measures like dietary sodium reduction, enhances outcomes without increasing adverse events in select populations. Overall, such targeted pharmacologic strategies in vulnerable groups can reduce progression to clinical hypertension and CVD complications by 20-40%, based on risk reductions observed in landmark trials and meta-analyses of RAS blockade.

Management

Treatment Goals and Guidelines

The 2025 (AHA)/ (ACC) guideline establishes a universal treatment goal of less than 130/80 mm Hg for all adults with hypertension, aiming to reduce () risk through early intervention and consistent monitoring. This target applies broadly, with therapy initiation recommended at 140/90 mm Hg or higher, or at 130/80 mm Hg for those with elevated 10-year (≥7.5%) as assessed by the PREVENT equations, which incorporate factors like function and use for improved stratification. For adults over 65 years, the guideline endorses a systolic target below 130 mm Hg if tolerated, emphasizing individualized assessment to balance benefits against potential harms such as . In patients with (), the goal remains less than 130/80 mm Hg (with systolic below 130 mm Hg), prioritizing renoprotective agents while monitoring for adverse events. Similarly, for those with , the target is less than 130/80 mm Hg (systolic below 130 mm Hg), supported by evidence of improved microvascular and macrovascular outcomes. The 2024 (ESC) guidelines align closely, recommending a target of less than 130/80 mm Hg for most hypertensive adults, with a preferred systolic range of 120-129 mm Hg to optimize CVD prevention without excessive risk. This framework incorporates risk stratification tools akin to PREVENT, such as SCORE2, to guide therapeutic decisions in high-risk groups, though it emphasizes office and home monitoring for accurate goal assessment. For elderly patients (including those over 65), the ESC advocates targets below 130/80 mm Hg if feasible, with adjustments for frailty and comorbidities to ensure tolerability. In CKD and , the guidelines maintain the less than 130/80 mm Hg goal, highlighting the need for personalized approaches to mitigate complications like progression of . Achieving tighter blood pressure control, as demonstrated in seminal trials like SPRINT, reduces major CVD events by approximately 25% compared to standard targets, underscoring the value of these guidelines in clinical practice. The World Health Organization's 2023 Global report on hypertension: the race against a silent killer emphasizes that hypertension is often asymptomatic until complications arise, describing it as a "silent killer." The report highlights that effective treatment and improved control rates could prevent millions of premature deaths and major cardiovascular events globally. Specifically, scaling up hypertension treatment to levels observed in high-performing countries could avert approximately 76 million deaths, 120 million strokes, 79 million heart attacks, and 17 million cases of heart failure between 2023 and 2050. These projections underscore the profound impact of adhering to evidence-based management strategies and achieving blood pressure control. Adherence monitoring is integral, with both AHA/ACC and ESC recommending regular follow-up using validated measurement techniques to evaluate progress and adjust therapy as needed.

Nonpharmacologic Interventions

Nonpharmacologic interventions are essential first-line strategies in the , particularly for patients with mild or stage 1 disease, and serve as adjuncts to pharmacologic in more severe cases. These approaches, including targeted modifications, can achieve meaningful reductions and improve overall cardiovascular health without the risks associated with medications. According to the 2025 / guidelines, all adults with hypertension should prioritize these interventions to reach treatment goals of less than 130/80 mm Hg. Dietary modifications, especially sodium restriction, form a foundational element. Limiting sodium intake to less than 2,300 mg per day, ideally 1,500 mg, by avoiding processed foods and table salt, can lower systolic blood pressure by 2-5 mm Hg across populations. The Dietary Approaches to Stop Hypertension (DASH) eating plan, which emphasizes 4–5 servings each of fruits and vegetables daily, along with whole grains, lean proteins, nuts, and low-fat dairy while limiting red meat, sweets, and added sugars, produces additive benefits; randomized trials show it reduces systolic blood pressure by 5-6 mm Hg compared to a standard diet, with effects amplified in hypertensive individuals to up to 11 mm Hg when combined with low-sodium intake, and similar benefits for diastolic pressure of 3-5 mm Hg. Weight management is particularly impactful for or obese patients, where excess adiposity contributes to hypertension . Intentional through caloric restriction and behavioral changes yields reductions proportional to the degree of loss; meta-analyses indicate approximately 1 mm Hg systolic decrease per lost, with modest reductions of 5-10 pounds (2-5 kg) if overweight associated with 5-10 mm Hg drops in systolic pressure, particularly when accompanied by decreases in waist circumference or central adiposity. The 2025 guidelines recommend aiming for a below 25 kg/m² to optimize these outcomes. Physical activity is another cornerstone, with guidelines endorsing at least 150 minutes per week of moderate-intensity , such as brisk walking, , or swimming, supplemented by 2–3 days of strength training and isometric exercises like wall sits or planks. Such regimens consistently lower systolic by 5-8 mm Hg in hypertensive adults, with comparable diastolic reductions, and benefits persisting long-term through improved endothelial function and reduced sympathetic activity. Alcohol moderation addresses a modifiable , as excessive intake elevates dose-dependently. Restricting consumption to no more than one per day for women and two for men can prevent rises and achieve reductions of 3-4 mm Hg systolic in heavy drinkers who cut back; complete is advised for those with uncontrolled hypertension. Smoking cessation is also recommended, as tobacco use exacerbates vascular damage and elevates blood pressure; quitting can contribute to overall reductions within weeks to months. Stress management techniques, including deep breathing, meditation, and yoga, further support blood pressure control by mitigating sympathetic activation. Vitamin D supplementation has been investigated as a potential nonpharmacologic intervention for hypertension. However, large meta-analyses and randomized controlled trials have shown that vitamin D supplementation, including high doses (e.g., 4000 IU/day or more), does not significantly lower blood pressure in the general population or most hypertensive patients. Some studies indicate possible modest benefits in specific subgroups, such as older adults with obesity or vitamin D deficiency, but high doses provide no additional benefit over standard doses, and overall evidence does not support its use as an antihypertensive therapy. For patients with persistent hypertension despite optimized lifestyle and multidrug therapy, device-based renal denervation provides a targeted option in select cases. This minimally invasive procedure uses catheter-delivered energy to ablate overactive renal sympathetic nerves, addressing neurogenic contributions to resistant hypertension. The U.S. Food and Drug Administration approved renal denervation systems in 2023, with endorsements in the 2025 hypertension guidelines for adults with uncontrolled blood pressure on three or more medications. Sham-controlled trials, including the SPYRAL HTN series, report durable systolic reductions of 6-9 mm Hg at 12 months and up to 3 years, with low procedural risks. Patient education is integral to the success of nonpharmacologic interventions, empowering individuals to adopt and sustain changes through knowledge of hypertension risks and techniques such as home blood pressure tracking. Educational programs improve adherence, enhance , and boost control rates by 10-20% in clinical settings; patients should consult healthcare providers to evaluate underlying causes or medication needs. In mild hypertension, these strategies alone can normalize and obviate the need for drugs in 20-30% of cases, underscoring their role in personalized management, with noticeable effects often emerging in weeks to months.

Pharmacologic Therapy

Pharmacologic therapy for hypertension targets key physiological mechanisms to reduce and cardiovascular risk. The primary antihypertensive drug classes include inhibitors (ACEIs) and angiotensin II receptor blockers (ARBs), which inhibit the renin-angiotensin-aldosterone system (RAAS) to decrease and sodium retention; (CCBs), particularly long-acting dihydropyridine types, which promote vascular relaxation and ; diuretics, such as and indapamide, which enhance sodium and water excretion to reduce plasma volume; and beta-blockers, which antagonize activity to lower and . According to the 2025 American Heart Association (AHA)/American College of Cardiology (ACC) guidelines, ACEIs, ARBs, CCBs, and thiazide diuretics are recommended as first-line agents (Class of Recommendation [COR] I, Level of Evidence [LOE] A), with selection guided by patient-specific factors such as comorbidities, age, and ethnicity. For stage 1 hypertension (blood pressure 130-139/80-89 mm Hg) in low-risk adults, monotherapy is typically initiated after lifestyle modifications, while stage 2 hypertension (≥140/90 mm Hg), particularly with initial readings >150/100 mm Hg, or stage 1 in high-risk individuals (e.g., with cardiovascular disease, diabetes, chronic kidney disease, or 10-year cardiovascular risk ≥7.5% via the PREVENT equation) warrants initial dual therapy to achieve prompt control. For such stage 2 cases, especially in young patients, dual therapy (particularly ARB + CCB) is recommended over monotherapy, as it achieves better and faster blood pressure control, whereas monotherapy often fails to provide rapid reductions in higher readings. Single-pill combinations (SPCs), such as an RAAS blocker paired with a CCB or thiazide diuretic, are strongly preferred for stage 2 and high-risk cases to improve adherence and efficacy (COR I, LOE A). Therapy must be individualized to optimize outcomes and minimize adverse effects. For example, in adults, diuretics or CCBs are preferred as monotherapy due to greater compared to RAAS inhibitors alone, which show reduced blood pressure-lowering response in this population (COR I, LOE A). Common side effects include dry cough and with ACEIs (affecting 5-20% and <0.1% of patients, respectively), with ARBs, and with thiazides, with CCBs, and fatigue or with beta-blockers; monitoring and dose adjustments are essential to manage these risks. The 2025 ACC highlights emerging options from recent trials, including aprocitentan, a dual that reduces systolic by 4-6 mm Hg when added to standard in resistant cases (from the PRECISION trial), and lorundrostat, an aldosterone synthase inhibitor that achieved significant systolic reductions versus at 12 weeks in the ADVANCE-HTN trial. These agents represent potential adjuncts, though established classes remain the cornerstone of .
Drug ClassMechanismFirst-Line UseKey Considerations
ACEIs/ARBsRAAS blockade reducing and aldosteroneYes (COR I, LOE A)Less effective monotherapy in Black patients; monitor renal function and potassium
CCBs (dihydropyridine)Vasodilation via calcium influx inhibitionYes (COR I, LOE A)Preferred in Black patients; effective for prevention
diuretics and reducing volumeYes (COR I, LOE A)Preferred in Black patients; monitor electrolytes
Beta-blockersSympathetic inhibition lowering Compelling indications (e.g., , post-MI)Not first-line generally; use in younger patients or with tachycardia

Resistant and Secondary Hypertension Management

Resistant hypertension is defined as above goal despite the concurrent use of three antihypertensive agents from different classes at maximally tolerated doses, including a long-acting dihydropyridine , a blocker of the renin-angiotensin system (such as an inhibitor or angiotensin receptor blocker), and a . This definition also encompasses controlled requiring four or more antihypertensive medications. It affects approximately 10% to 20% of patients with hypertension, with population-based studies estimating prevalence at 12% to 15% among treated individuals. The condition is associated with higher cardiovascular risk, necessitating thorough evaluation to distinguish true resistance from pseudoresistance. Evaluation begins with confirming adherence to prescribed , as nonadherence accounts for up to 50% of apparent resistant cases; methods include pill counts, records, or direct observation. Out-of-office monitoring, such as or measurements, is essential to exclude white-coat hypertension, which can mimic resistance in clinic settings. Screening for secondary causes is critical, involving targeted history, , and laboratory tests for conditions like , , or . Lifestyle factors, including high sodium intake, , and excessive alcohol use, should be addressed concurrently. Management of resistant hypertension prioritizes optimization of pharmacologic , starting with verification of dosing and adherence, followed by the addition of a such as , which reduces by 10 to 20 mm Hg systolic in responsive patients. For persistent elevation, device-based interventions like catheter-based renal denervation have gained endorsement in the 2025 ACC/AHA hypertension guidelines as an adjunctive option for patients with uncontrolled despite and medical , demonstrating sustained reductions of 5 to 10 mm Hg systolic at 36 months in clinical trials. Emerging therapies include (siRNA) agents like zilebesiran, which inhibits hepatic angiotensinogen synthesis and has shown reductions of up to 20 mm Hg systolic with quarterly dosing in phase II trials, advancing to global phase III studies in 2025 for resistant cases. Secondary hypertension, comprising 5% to 10% of all hypertension cases, requires identification and targeted treatment of the underlying etiology to achieve optimal control. Common causes include renal parenchymal disease, renovascular stenosis, and endocrine disorders; management involves specific interventions such as surgical correction for or aldosterone antagonists for , often leading to cure or significant improvement when addressed early. In parallel, antihypertensive medications and lifestyle modifications are used to maintain control until the primary cause is resolved. Multidisciplinary referral to specialists, such as endocrinologists or nephrologists, is recommended for comprehensive evaluation and therapy.

Epidemiology

Global and Regional Prevalence in Adults

Hypertension is known as the "silent killer" because it is often asymptomatic until severe complications occur, including stroke, heart attack, heart failure, kidney damage, and premature death. Hypertension affects 1 in 3 adults worldwide (approximately 1.3 billion people as of 2019 data). This burden is disproportionately concentrated in low- and middle-income countries (LMICs), where more than three-quarters of adults with hypertension reside, driven by factors such as , aging, and socioeconomic transitions. Regionally, prevalence varies significantly; for instance, rates reach up to 46% in and 38% in the WHO Region, compared to 29% in the Western Pacific Region. Demographic patterns reveal distinct risks by , age, and . is generally similar between sexes overall (34% in men and 32% in women aged 30–79 years), but men under 50 years exhibit higher rates, while women over 65 years show elevated due to postmenopausal changes. Ethnic disparities are pronounced globally, with individuals of African descent facing higher rates—for example, 58% among non-Hispanic adults compared to 49% in non-Hispanic adults (2021–2023). Awareness and control remain alarmingly low, with nearly half of adults with hypertension unaware globally, approximately 54% diagnosed, only 42% receiving treatment, and just 21% achieving control ( <140/90 mmHg). Control rates in LMICs are poor, around 10% in some studies. These gaps contribute to rising trends, particularly in urbanizing areas of LMICs, where rapid has been linked to increased prevalence through lifestyle shifts like reduced and higher salt intake. The WHO's 2023 report emphasizes that effective treatment could prevent millions of deaths, strokes, and heart attacks between 2023 and 2050.

Epidemiology in Children

Hypertension in children, defined as sustained levels at or above the 95th percentile for age, sex, and height, affects approximately 6.5% of children and adolescents worldwide as of 2020, nearly doubling from 3.4% in 2000 according to a 2025 . In the United States, prevalence estimates are around 4.5%, with elevated noted in an additional 10% to 15% of . Among obese adolescents, rates are notably higher, reaching up to 10%, driven by the strong association between excess adiposity and elevated . Unlike in adults, where primary ( predominates, pediatric cases are often secondary, particularly in younger children, with underlying causes such as renal disorders, , or endocrine abnormalities accounting for 45% to 85% of diagnosed instances in referral settings. Over the last 30–40 years, the prevalence of pediatric hypertension in the U.S. has risen fourfold, paralleling the epidemic that has tripled rates of childhood and . This upward trend is attributed to factors including sedentary , high-sodium diets, and increased caloric intake, with meta-analyses confirming increases linked directly to rising . Ethnic disparities exacerbate these patterns; for instance, non-Hispanic Black children exhibit higher rates of hypertension and abnormal nocturnal compared to White peers, even after adjusting for , while Hispanic boys show elevated prevalence independent of . Childhood hypertension tracks into adulthood, significantly elevating the risk of , including , , and coronary , with longitudinal studies demonstrating a 40% to 50% increased mortality risk from heart disease over decades. Recent 2025 global data confirm a continued rise, with hypertension prevalence reaching 6.53% among children and adolescents by 2020, particularly in youth, underscoring the impact of the global epidemic. Early identification through routine monitoring is thus critical to mitigate long-term sequelae.

Prognosis and Complications

Long-Term Prognosis

Effective (BP) control in patients with hypertension can substantially improve long-term survival outcomes, approaching that of normotensive individuals by mitigating the excess (CVD) risk associated with elevated BP. In contrast, uncontrolled hypertension significantly worsens , roughly doubling the risk of CVD mortality compared to well-managed cases, primarily due to accelerated vascular damage and event progression. The duration and severity of hypertension are critical determinants of long-term , with prolonged exposure to elevated levels leading to cumulative organ damage and higher lifetime CVD event rates, independent of current control status. For instance, patients with long-standing severe hypertension (e.g., stage 2 or higher) exhibit poorer survival trajectories than those with shorter duration or milder elevations, even after initiating treatment. Antihypertensive treatment yields meaningful risk reductions, with effective BP lowering associated with approximately a 25-30% decrease in 10-year CVD risk across diverse populations, highlighting the value of early and sustained intervention. This benefit is most pronounced in younger patients and those without advanced comorbidities, where therapy can extend event-free life years by several months to years. Landmark data from the demonstrate that each 20 mm Hg increase in systolic BP or 10 mm Hg increase in diastolic BP doubles the risk of CVD events and mortality, establishing a continuous, graded relationship from normal levels upward. Recent advancements, such as the 2025 PREVENT equations endorsed by the , further refine these predictions by incorporating contemporary risk factors like social determinants and metabolic variables for more accurate 10-year CVD forecasting in hypertensive individuals.

Associated Cardiovascular and Other Complications

Chronic hypertension exerts deleterious effects on multiple organ systems, primarily through sustained hemodynamic stress that damages vascular , promotes , and induces structural remodeling. This leads to end-organ damage, with cardiovascular complications being the most prominent, accounting for the majority of hypertension-related morbidity and mortality. Key mechanisms include , , and activation of the renin-angiotensin-aldosterone system, which exacerbate vascular stiffness and plaque formation. Globally, uncontrolled hypertension contributes to over 10 million deaths annually, representing a significant portion of cardiovascular mortality. Among cardiovascular complications, is one of the most common, with hypertension implicated in approximately 51% of deaths worldwide due to accelerated in and increased leading to rupture or occlusion. The risk follows a dose-response relationship, where levels exceeding 140/90 mmHg elevate incidence 2- to 4-fold compared to optimal levels, primarily through ischemic and hemorrhagic subtypes. (MI) risk is similarly heightened by hypertension, which promotes coronary artery and , increasing susceptibility to plaque rupture; antecedent hypertension is associated with higher in-hospital and long-term mortality post-MI. develops through chronic pressure overload causing and eventual systolic/diastolic dysfunction, with hypertension accounting for up to 76% of incident cases in recent decades; effective control can reduce incidence by 64%. Aortic and cerebral aneurysms are also accelerated by hypertension, which elevates wall tension and promotes degenerative changes in the vessel media, raising the risk of formation by 66% and rupture through hemodynamic stress. Beyond , hypertension accelerates (CKD) progression by inducing glomerular hyperfiltration, afferent arteriolar hypertrophy, and interstitial fibrosis, which worsen renal function decline; hypertension is present in over 80% of CKD patients and independently predicts faster progression to end-stage renal disease. arises from retinal arteriolar narrowing, cotton-wool spots, and hemorrhages due to breakdown of the blood-retinal barrier under elevated pressure, with prevalence ranging from 28.5% to 77.1% in hypertensive populations and serving as a marker of systemic microvascular damage. Dementia risk is elevated in midlife hypertension through cerebral small vessel disease, hyperintensities, and impaired cerebral blood flow autoregulation, conferring a 1.19- to 1.55-fold increased risk of and all-cause dementia.

History

Early Recognition and Measurement

The earliest recognition of phenomena related to dates back to ancient times, when (circa 460–370 BCE) described variations in the arterial as a vital sign indicative of health conditions such as fever and , laying foundational observations for later understandings of circulatory dynamics. These assessments, though not quantitative measurements of , represented an initial clinical awareness of blood flow irregularities that could signal hypertension-like states. A significant advancement occurred in the with the first direct measurement of , conducted by English clergyman and scientist in 1733. Hales inserted a brass cannula into the of a and connected it to a glass tube filled with fluid, observing the height to which the blood rose under arterial pressure, thereby quantifying systolic for the first time. This invasive experiment, detailed in Hales' work Haemastatics, established the principle of pressure as a measurable force in the vascular system and influenced subsequent physiological research. In the , French physician contributed foundational insights into through his studies on in narrow tubes, published between 1840 and 1846. Poiseuille's law described how resistance to flow in blood vessels depends on factors such as vessel radius, length, and blood viscosity, providing a theoretical basis for understanding pressure gradients essential to hypertension. This work paved the way for non-invasive measurement techniques, culminating in 1896 when Italian physician Scipione Riva-Rocci introduced the mercury , an upper-arm cuff device that compressed the to estimate systolic pressure via a mercury column. Riva-Rocci's invention marked a practical shift toward clinical applicability, though it initially measured only systolic pressure. The development of the auscultatory method in 1905 by Russian physician Nikolai Sergeyevich Korotkov enabled comprehensive non-invasive assessment. By listening with a during cuff deflation, Korotkov identified characteristic sounds—now known as —arising from turbulent blood flow, allowing differentiation between systolic and diastolic pressures. This innovation, validated through clinical trials, transformed hypertension diagnosis by making routine, accurate measurements feasible in medical practice.

Evolution of Understanding and Treatment

In the mid-20th century, experimental work laid foundational insights into the etiology of hypertension, particularly its renal origins. In 1934, Harry Goldblatt developed the first animal model of hypertension by partially clamping the renal arteries in dogs, demonstrating that renal ischemia could induce sustained high and elucidating the role of the renin-angiotensin system in its pathogenesis. This model, refined through subsequent studies in the 1940s, enabled researchers to isolate renin from extracts and establish the 's central role in certain forms of . Concurrently, the , initiated in 1948, provided epidemiological evidence linking hypertension to cardiovascular risks, identifying it as a primary modifiable factor for heart disease, stroke, and through long-term cohort analysis. The 1950s marked the advent of pharmacologic interventions, shifting hypertension from an untreatable condition to one amenable to therapy. , derived from the Rauwolfia serpentina plant, was introduced as one of the first effective antihypertensives, acting centrally to deplete catecholamines and reduce sympathetic outflow, though its use was limited by side effects like depression. , a direct vasodilator, emerged around the same time, targeting arteriolar to lower peripheral resistance, often combined with other agents to mitigate reflex . These drugs, validated in early clinical trials such as the Veterans Administration Cooperative Study, demonstrated that treating severe hypertension could prevent and , paving the way for broader therapeutic adoption. By the 1970s, advances in understanding the renin-angiotensin-aldosterone system spurred more targeted therapies. Beta-blockers, such as introduced in the late 1960s and widely applied to hypertension by the 1970s, reduced cardiac output and renin release, proving effective in reducing cardiovascular events in trials like the Beta-Blocker Heart Attack Trial. inhibitors (ACEIs), exemplified by —developed from peptides and approved in 1981—blocked angiotensin II formation, offering renoprotective benefits alongside blood pressure reduction, as shown in the CONSENSUS trial for patients with hypertension. These developments coincided with the evolution of clinical guidelines; the first Joint National Committee (JNC) report in 1977 recommended treating diastolic pressures above 90 mm Hg, evolving through subsequent iterations to emphasize systolic control and combination therapy. The 2025 (AHA)/ (ACC) guideline further refined this, setting a uniform treatment target of less than 130/80 mm Hg for most adults while incorporating risk stratification. Entering the 21st century, precision medicine has transformed hypertension management by leveraging for individualized therapy. Pharmacogenomic approaches, such as for variants in genes like ADRB1 or , enable tailored selection of beta-blockers or ACEIs, improving response rates and reducing adverse effects, as evidenced in studies like the PEAR trial. By 2025, (siRNA) therapies represent a milestone in long-acting treatments; zilebesiran, an investigational siRNA targeting hepatic angiotensinogen synthesis, has shown sustained reductions for up to six months after a single subcutaneous dose in phase 2 trials, with phase 3 studies underway to assess cardiovascular outcomes. These innovations underscore a shift toward etiology-specific interventions, building on decades of causal elucidation and guideline refinement to enhance control rates globally.

Society and Culture

Public Awareness and Screening

Public awareness campaigns play a crucial role in addressing hypertension, a condition often termed the "silent killer" due to its asymptomatic nature in early stages. The World Hypertension League (WHL), in collaboration with the World Health Organization (WHO), launched World Hypertension Day on May 14, 2005, with annual observances on May 17 starting in 2006, to promote global awareness of high blood pressure and encourage regular blood pressure measurements. This annual event, observed on May 17 each year, features educational activities, free screening events, and media campaigns aimed at highlighting the importance of early detection and lifestyle modifications to prevent complications. In 2025, the 20th anniversary of World Hypertension Day emphasized the theme "Measure Your Blood Pressure Accurately, Control It, Live Longer," aligning with broader WHO efforts to integrate hypertension awareness into noncommunicable disease prevention strategies. In the United States, the Million Hearts initiative, launched in 2011 by the Department of Health and Human Services and the Centers for Disease Control and Prevention (CDC), targets preventing one million heart attacks and strokes by focusing on hypertension control through public education and clinical recognition. The program promotes awareness via the Hypertension Control Champions recognition, which honors high-performing health systems and clinicians achieving control rates above 80% in their patient populations. Complementing these efforts, community-based screening programs, such as the "Take the Pressure Off, NYC!" initiative in , establish monitoring stations in everyday locations like pharmacies, churches, and markets to reach underserved populations and facilitate timely referrals to care. Workplace wellness initiatives have also expanded, with employers implementing on-site screenings to detect hypertension among employees, particularly young adults, as part of broader cardiovascular health programs. The rise of digital tools has further enhanced screening accessibility, especially by 2025, with mobile health () applications enabling of through connected devices and providing real-time feedback integrated with consultations. These apps, often incorporating AI-driven educational content, have seen increased adoption in both high- and low-resource settings, supporting remote patient engagement and bridging gaps in traditional healthcare access. Despite these advances, significant disparities persist, with the largest gaps in low- and middle-income where only about half of adults with hypertension are aware of their condition, compared to over 80% in high-income nations. targets, including the WHO's HEARTS initiative, aim for 80% screening coverage by 2025 as part of the "80-80-80" cascade—ensuring 80% of adults are screened, 80% of those diagnosed receive treatment, and 80% achieve control—to avert millions of cardiovascular deaths. However, as of 2025, global progress lags, with only 23% of adults with hypertension having controlled .

Economic Burden and Policy Implications

The economic burden of hypertension encompasses such as healthcare expenditures and medications, as well as including lost from premature and death. Globally, cardiovascular diseases—including hypertension—are projected to cost low- and middle-income countries approximately US$3.7 trillion from 2011 to 2025, equivalent to about 2% of their combined . In the United States, imposes an annual economic burden of $131 billion, covering medical care, prescription drugs, and losses. These costs highlight the scale of the challenge, with hypertension contributing to substantial and reduced economic output in affected populations. An estimated 80% of cardiovascular diseases attributable to hypertension are preventable through interventions, early detection, and effective , underscoring the potential for cost savings via strategies. Productivity losses alone represent a significant portion of the total burden, as uncontrolled hypertension leads to complications that impair work capacity and increase disability-adjusted life years lost. Policy responses worldwide focus on reducing these costs through targeted initiatives and financial incentives. National programs, such as China's Rural Hypertension Control Project, deploy low-cost, community-based models led by village doctors to enhance screening, treatment, and control in rural areas. Subsidies for generic antihypertensive drugs, including single-pill combinations, have been implemented to improve affordability, boost adherence, and lower overall healthcare spending. In 2025, updated international guidelines and policies prioritize equity in access, aiming to address disparities in care delivery for low-income and marginalized groups to achieve more inclusive hypertension .

Other Animals

Hypertension in Veterinary Medicine

Hypertension, defined as sustained elevation in systemic , is a significant clinical concern in , particularly among companion animals such as dogs and cats. It is most commonly secondary to underlying conditions like (CKD) and in cats, and CKD or hyperadrenocorticism in dogs. In older cats, the prevalence can reach 20-65%, especially those with CKD, where it exacerbates renal damage and contributes to target organ injury. Clinical recognition often involves identifying signs of target organ damage, including ocular manifestations such as and hemorrhage leading to acute blindness, as well as neurological symptoms like disorientation or seizures. Diagnosis of hypertension in veterinary patients employs noninvasive techniques similar to those in human medicine, including Doppler sphygmomanometry and oscillometric devices, with multiple readings recommended to account for stress-induced elevations. Species-specific reference ranges are essential; for dogs, a systolic (SBP) below 160 mmHg is generally considered normal, while values exceeding this threshold warrant investigation for hypertension. In cats, an SBP greater than 160 mmHg is often used as a diagnostic cutoff, though persistent readings above 140 mmHg may indicate preclinical . Routine screening is advised for at-risk populations, such as senior cats with CKD or , to enable early intervention. Treatment focuses on managing the underlying cause where possible, alongside antihypertensive to mitigate organ damage. Amlodipine, a , is the first-line treatment for feline hypertension, typically administered at 0.625-1.25 mg per once daily, effectively lowering SBP by 30-60 mmHg in most cases. For dogs, () inhibitors like enalapril (0.5 mg/kg twice daily) are often preferred initially, with amlodipine added if needed for refractory cases. While systemic hypertension is less commonly reported in farm animals, where predominates in species like at high altitudes, management in companions parallels approaches in emphasizing control to improve and .

Comparative Pathophysiology

Comparative pathophysiology of hypertension examines the mechanisms underlying elevated across species, highlighting similarities and divergences that inform human research by revealing conserved pathways and species-specific adaptations. In mammals, hypertension often involves dysregulation of the renin-angiotensin-aldosterone system (RAAS), , and vascular remodeling, mechanisms that parallel human but vary in prevalence and triggers depending on evolutionary pressures and . Rodent models, particularly the Dahl salt-sensitive rat, have been instrumental in elucidating salt-induced hypertension mechanisms. Developed by in the , this strain exhibits profound elevation on high-salt diets due to impaired renal sodium , heightened sympathetic activity, and RAAS overactivation, mimicking salt-sensitive hypertension. These models demonstrate genetic susceptibility loci on chromosomes influencing and vascular tone, providing a platform for dissecting polygenic contributions absent in monogenic strains. Nonhuman primates, such as the African green monkey (Chlorocebus aethiops) and cynomolgus macaque, offer closer approximations to human RAAS dynamics, with spontaneous hypertension occurring in 5-15% of feral populations linked to genetic and dietary factors. Unlike , primates show more human-like renal vascular pathologies, including arteriolar thickening and glomerular ischemia, under chronic RAAS activation, reflecting greater evolutionary conservation in signaling and aldosterone responsiveness. This similarity facilitates translation of RAAS-targeted interventions, as primate models replicate human endothelial dysregulation more accurately than smaller mammals. Birds diverge markedly, lacking the spontaneous systemic hypertension prevalent in mammals; instead, they predominantly experience , as seen in chickens under hypoxic or rapid-growth conditions leading to and . This absence of typical systemic hypertension stems from avian circulatory adaptations, contrasting with mammalian trends. Evolutionary pressures in birds favor efficient oxygen delivery over high systemic pressures. In large mammals, evolutionary adaptations mitigate hydrostatic challenges from increased body size, resulting in baseline hypertension to maintain organ perfusion against ; for instance, giraffes sustain mean arterial pressures around 200 mmHg through elongated vascular structures and enhanced RAAS tone, preventing orthostatic failure. This scaling of with mass—rising approximately 10 mmHg per decade of body mass increase—highlights gravitational selection as a driver, differing from smaller where such pressures would induce organ damage. These adaptations underscore why hypertension pathology in large mammals more closely informs human cardiovascular strain than in smaller vertebrates. The RAAS exhibits approximately 80% genetic conservation across mammals, enabling cross-species modeling of hypertension pathways from angiotensinogen synthesis to aldosterone secretion. This homology has propelled advancements, including 2025 siRNA therapies targeting hepatic angiotensinogen in models, which achieved sustained reduction for up to six months without significant adverse effects, bridging preclinical insights to applications.

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