Essential hypertension

Essential hypertension (also called primary hypertension, or idiopathic hypertension) is a form of hypertension without an identifiable physiologic cause. It is the most common type affecting 85% of those with high blood pressure. The remaining 15% is accounted for by various causes of secondary hypertension. Essential hypertension tends to be familial and is likely to be the consequence of an interaction between environmental and genetic factors. Hypertension can increase the risk of cerebral, cardiac, and renal events.

Blood pressure is classified as normal blood pressure, prehypertension, hypertension (stages I and II), and isolated systolic hypertension, which is a common occurrence among the elderly. These readings are based on the average of seated blood pressure readings that were properly measured during 2 or more office visits. In adults, hypertension is considered to be present when a person's blood pressure is consistently at least 140 mmHg systolic or 90 mmHg diastolic. Patients with blood pressures over 130/80 mmHg along with Type 1 or Type 2 diabetes, or kidney disease require further treatment.

Resistant hypertension is defined as the failure to reduce blood pressure to normal levels following an adequate trial of three antihypertensive medications. Guidelines for treating resistant hypertension have been published in the UK, and US.

The etiology of hypertension differs widely amongst individuals within a large population. While essential hypertension has no identifiable cause, several risk factors have been identified.

Having a personal family history of hypertension increases the likelihood that an individual develops it. More than 50 genes have been examined in association studies with hypertension, and the number is constantly growing. One of these genes is the angiotensinogen (AGT) gene, studied extensively by Kim et al. They showed that increasing the number of AGT increases the blood pressure and hence this may cause hypertension. In single variant tests, it has been shown that SNPs were enriched for variants associated with adiposity, type 2 diabetes, coronary heart disease and kidney function in previously published GWAS, providing evidence that genetic loci related to blood pressure contribute to cardiovascular outcomes. Twins have been included in studies measuring ambulatory blood pressure; from these studies it has been suggested that there is a large genetic influence on essential hypertension. Supporting data has emerged from animal studies as well as clinical studies in human populations. The majority of these studies support the concept that the inheritance is probably multifactorial or that a number of different genetic defects each has an elevated blood pressure as one of its phenotypic expressions. However, the genetic influence on hypertension is not fully understood at the moment. It is believed that linking hypertension-related phenotypes with specific variations of the genome may yield definitive evidence of heritability. Another view is that hypertension can be caused by mutations in single genes, inherited on a Mendelian basis.

In the United States, essential hypertension is four times more common in black than white people, accelerates more rapidly and is often more severe with higher mortality in black patients. It is argued there are numerous racial inequities, often inconspicuous, that contribute to black individuals having higher prevalence of essential hypertension than white people. Discrimination may have both a direct and indirect effect on hypertension. Chronic stress, like that caused by perceived discrimination, has been linked to a number of health problems. Access to social, financial, and educational resources that can enhance one's health is unequally impacted by racial prejudice. Numerous studies have demonstrated the connection between feeling discriminated against and having elevated blood pressure. In comparison to participants who reported low levels of lifetime discrimination, a study from the Jackson Heart Study indicated that those people who reported high or medium levels of prejudice were more likely to acquire hypertension. Racial inequities are rarely acknowledged as significant risk factors in the healthcare industry.

Other studies have noted while African-Americans tend to have elevated hypertension relative to the general American population, their rates of high blood pressure are nonetheless much lower than some other white populations globally. Russians and eastern Europeans have markedly higher hypertension rates than Black Americans, and blood pressure rates vary substantially among black Africans with obesity rates being closely correlated with hypertension.

An unhealthy diet, which includes excessive consumption of unhealthy food, is a recognized risk factor for hypertension. A balanced diet is recommended for both its prevention and control. Dietary sodium intake also contributes to blood pressure. Approximately one third of the essential hypertensive population is responsive to sodium intake. When sodium intake exceeds the capacity of the body to excrete it through the kidneys, blood volume will expand due to movement of fluids by osmosis into the blood vessels. This causes the arterial pressure to rise as the cardiac output will increase. Local autoregulatory mechanisms counteract this by increasing the vascular resistance to blood flow in order to maintain normal pressure in the capillary blood vessels . As arterial pressure increases in response to high sodium chloride intake, urinary sodium excretion increases but this higher excretion of salt is maintained at the expense of increased arterial blood pressure. The increased sodium ion concentration stimulates ADH and thirst mechanisms, leading to increased reabsorption of water in the kidneys, a concentrated urine, and thirst with a higher intake of water.