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Nitrovasodilator
Nitrovasodilator
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Nitrovasodilator
Drug class
Nitric oxide
Class identifiers
UseAngina pectoris, vasodilation
ATC codeC01DA
Biological targetGuanylate cyclase
Legal status
In Wikidata

A nitrovasodilator is a pharmaceutical agent that causes vasodilation (widening of blood vessels) by donation of nitric oxide (NO),[1] and is mostly used for the treatment and prevention of angina pectoris.

This group of drugs includes nitrates (esters of nitric acid), which are reduced to NO in the body, as well as some other substances.

Examples

[edit]

Here is a list of examples of the nitrate type (in alphabetical order):[2]

  1. Diethylene glycol dinitrate
  2. Glyceryl trinitrate (nitroglycerin)
  3. Isosorbide mononitrate and dinitrate
  4. Itramin tosilate
  5. Nicorandil (which additionally acts as a potassium channel opener)
  6. Pentaerithrityl tetranitrate
  7. Propatylnitrate
  8. Sinitrodil
  9. Tenitramine
  10. Trolnitrate

Nitrovasodilators which aren't nitrates include molsidomine and its active metabolite linsidomine, as well as sodium nitroprusside. These substances do not need to be reduced to donate NO.[2][3]

Medical uses

[edit]
Glyceryl trinitrate (nitroglycerine)
Molsidomine
Sodium nitroprusside

The nitrates are used for the treatment and prevention of angina and acute myocardial infarction, while molsidomine acts too slowly to be useful for the treatment of acute angina.[2] For quick action in the treatment of angina, glyceryl trinitrate is used in form of a sublingual spray (nitro spray) or as soft capsules to be crunched.[4]

Nitroprusside is used intravenously for the treatment of hypertensive crises, heart failure, and lowering of blood pressure during surgery.[5][6]

Contraindications

[edit]

Nitrovasodilators are contraindicated under circumstances where lowering of blood pressure can be dangerous. This includes, with some variation between the individual substances, severe hypotension (low blood pressure), shock including cardiogenic shock, and anaemia. Whether a specific drug is useful or harmful under heart failure and myocardial infarction depends on its speed of action: Fast acting substances such as glyceryl trinitrate and nitroprusside can be helpful for controlling blood pressure and consequently the amount of blood the heart has to pump, if the application is monitored continuously. Slow acting substances would hold the danger of ischaemia due to an uncontrollably low blood pressure and are therefore contraindicated. Depending on the circumstances, even fast acting substances can be contraindicated – for example, glyceryl trinitrate in patients with obstructive heart failure.[2][4]

These drugs are also contraindicated in patients that have recently taken PDE5 inhibitors such as sildenafil (Viagra).[4]

Adverse effects

[edit]

Most side effects are direct consequences of the vasodilation and the resultant low blood pressure. They include headache ("nitrate headache") resulting from the widening of blood vessels in the brain, reflex tachycardia (fast heart rate), flush, dizziness, nausea and vomiting. These effects usually subside after a few days if the treatment is continued.[2]

Occasionally, severe hypotension occurs shortly after beginning of treatment, possibly resulting in intensified angina symptoms or syncope, sometimes with bradycardia (slow heart rate).[4]

Interactions

[edit]

A number of drugs add to the low blood pressure caused by nitrovasodilators: for example, other vasodilators, antihypertensive drugs, tricyclic antidepressants, antipsychotics, general anaesthetics, as well as ethanol. Combination with PDE5 inhibitors, including sildenafil (Viagra), is contraindicated because potentially life-threatening hypotension may occur.[2][4]

Nitrates increase the bioavailability of dihydroergotamine (DHE). High DHE levels may result in coronary spasms in patients with coronary disease.[4] This interaction is not described for non-nitrate nitrovasodilators.

Mechanism of action

[edit]

Nitrovasodilators are prodrugs that donate NO by various mechanisms. Nitrates undergo chemical reduction, likely mediated by enzymes. Molsidomine and nitroprusside already contain nitrogen in the right oxidation state (+2) and liberate NO without the aid of enzymes.[3]

NO stimulates the soluble form of the enzyme guanylate cyclase in the smooth muscle cells of blood vessels. Guanylate cyclase produces cyclic guanosine monophosphate (cGMP) from guanosine triphosphate (GTP). cGMP in turn activates cyclic nucleotide-dependent protein kinase G, which phosphorylates various proteins that play a role in decreasing intracellular calcium levels, leading to relaxation of the muscle cells and thus to dilation of blood vessels.[3][7]

The most important effect in angina is the widening of veins, which increases their capacity to hold blood ("venous pooling") and reduces the pressure of the blood returning to the heart (the preload). Widening of the large arteries also reduces the pressure against which the heart has to pump, the afterload. Lower preload and afterload result in the heart needing less energy and thus less oxygen. Besides, NO donated by nitrovasodilators can reduce coronary spasms, increasing the heart's oxygen supply.[2]

PDE5 inhibitors block deactivation of cGMP by the enzyme phosphodiesterase-5. In combination with the increased cGMP production caused by nitrovasodilators, this leads to high concentrations of cGMP, extensive venous pooling, and potentially life-threatening hypotension.[8][9]

Nitrate tolerance

[edit]

Nitrates exhibit development of tolerance, or more specifically tachyphylaxis, meaning that repeated application results in a fast decrease of effect, usually within 24 hours. A pause of six to eight hours restores the original effectiveness. This phenomenon was originally thought to be a consequence of depletion of thiol (–SH) groups necessary for the reduction of nitrates. While this theory would fit the fact that molsidomine (which is not reduced) does not exhibit tachyphylaxis, it has meanwhile been refuted. Newer theories include increase of oxidative stress resulting in deactivation of NO to peroxynitrite, and liberation of the vasoconstrictors angiotensin II and endothelin as the blood vessels' reaction to NO-mediated vasodilation.[2]

Differences in pharmacokinetics

[edit]

Nitrates mainly differ in speed and duration of their action. Glyceryl trinitrate acts fast and short (10 to 30 minutes), while most other nitrates have a slower onset of action, but are effective for up to six hours. Molsidomine, as has been mentioned, not only acts slowly but also differs from the nitrates in exhibiting no tolerance.[2] Nitroprusside, given intravenously, acts immediately, and after stopping the infusion blood pressure returns to its previous level within ten minutes.[6]

See also

[edit]

References

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Nitrovasodilator

View on Grokipedia
from Grokipedia
A nitrovasodilator is a pharmaceutical agent that induces by donating (NO), a potent endogenous signaling molecule that relaxes vascular cells. These compounds encompass organic nitrates, such as (glyceryl trinitrate) and , as well as metal-containing agents like . By releasing NO, nitrovasodilators activate soluble in cells, elevating (cGMP) levels, which dephosphorylates light chains and reduces intracellular calcium, thereby promoting arterial and venous dilation. Clinically, nitrovasodilators are cornerstone therapies for cardiovascular conditions, particularly pectoris, where short-acting formulations like sublingual (0.3–0.6 mg) provide rapid relief by dilating and decreasing myocardial oxygen demand through preload reduction. They are also employed in acute to lower and improve via balanced arterial and venous effects, and in hypertensive emergencies with agents like for controlled reduction. Long-acting nitrates, such as (60–240 mg daily), serve as second-line prophylaxis for chronic stable after beta-blockers or . Despite their efficacy, nitrovasodilators are associated with common adverse effects including (incidence >10%, up to 64%), flushing, , and due to systemic . A major limitation is the development of tolerance with continuous exposure (after 12–24 hours), attributed to impaired and , which can be mitigated by implementing nitrate-free intervals of 8–10 hours. Ongoing explores strategies to enhance NO bioavailability and overcome tolerance for broader therapeutic applications.

General Overview

Definition and Classification

Nitrovasodilators are a class of pharmaceutical agents that induce vasodilation primarily through the donation of nitric oxide (NO), which activates soluble guanylate cyclase in vascular smooth muscle cells, leading to increased cyclic guanosine monophosphate (cGMP) levels and subsequent relaxation of smooth muscle. This NO-mediated mechanism reduces preload and afterload, distinguishing nitrovasodilators from other vasodilator classes that act via different pathways, such as calcium channel blockade. Nitrovasodilators are broadly classified into organic nitrates and other nitro compounds based on their and NO-releasing properties. Organic nitrates, the most common subclass, contain the characteristic nitrate ester group (R-ONO₂), exemplified by (glyceryl trinitrate) and , which require enzymatic bioactivation—primarily by mitochondrial aldehyde dehydrogenase-2 ()—to liberate NO. In contrast, other nitro compounds, such as , function as direct or spontaneous NO donors without needing bioactivation, releasing NO rapidly upon administration. This classification highlights their shared vasodilatory endpoint but differing and clinical handling. A key property of most nitrovasodilators, particularly organic nitrates, is the necessity for bioactivation to generate bioactive NO species, such as through denitration reactions that produce intermediates, which sets them apart from pure direct NO donors like gaseous NO or certain metal nitrosyl complexes. This bioactivation step is crucial for their therapeutic efficacy but can contribute to challenges like tolerance upon prolonged exposure.

Historical Development

The synthesis of , a prototypical nitrovasodilator, occurred in 1847 when Italian chemist produced it by nitrating with a mixture of nitric and sulfuric acids while working in under Théophile-Jules Pelouze. Sobrero recognized its explosive potential but also noted its physiological effects, including severe headaches indicative of vasodilatory action, though he deemed it too unstable for practical medical application at the time. Early explorations of its biological properties began in the mid-19th century, with homeopathic uses reported as early as 1849 by Constantin Hering, who administered small doses to induce controlled headaches. The therapeutic potential of nitrovasodilators for cardiovascular conditions emerged in the 1860s, driven by efforts to alleviate pectoris. In 1867, Scottish physician Thomas Lauder Brunton pioneered the clinical use of , an organic nitrite, to relieve anginal pain through , marking the first targeted application of a in . Building on this, British physician William Murrell extended the approach to in 1879, administering it to patients with and after observing its blood pressure-lowering effects in healthy volunteers; his work led to its inclusion in the by 1892. These developments established nitrovasodilators as key agents for symptom relief in , with transitioning from an industrial explosive—famously stabilized by for production in the 1860s—to a medical staple. Throughout the , nitrovasodilators saw widespread clinical adoption for treating cardiovascular diseases, including , , and , due to their rapid vasodilatory effects on coronary and systemic vessels. Sublingual tablets, in use since the early 20th century, received initial U.S. (FDA) approval in 1981 for specific formulations, formalizing their use for acute relief and enabling broader accessibility. A pivotal advancement came in 1977 when pharmacologist demonstrated that nitrovasodilators like release (NO), which activates guanylyl cyclase in vascular to produce cyclic GMP and induce relaxation, elucidating their mechanism at the molecular level. This finding connected organic nitrates to endogenous NO signaling, reinforced by Robert Furchgott's 1980 discovery of (EDRF) and the 1987 confirmation by and that EDRF is NO, which collectively transformed understanding of vascular biology. By the 1980s, as long-acting nitrovasodilator formulations proliferated for chronic therapy, clinicians recognized the phenomenon of nitrate tolerance, where prolonged exposure diminishes vasodilatory efficacy, often necessitating dose adjustments or nitrate-free intervals to restore responsiveness. This insight, emerging from studies on sustained use, refined dosing strategies and highlighted and neurohormonal activation as underlying causes, ensuring safer long-term application in cardiovascular management.

Clinical Applications

Medical Uses

Nitrovasodilators are primarily employed for the acute relief of pectoris in patients with , where they rapidly reduce myocardial oxygen demand by dilating coronary arteries and peripheral veins. For instance, sublingual is a first-line agent for terminating acute attacks, providing symptom relief within minutes by decreasing preload and . They also serve to prevent attacks through long-term use, with oral commonly prescribed for chronic stable to improve exercise tolerance and reduce the frequency of ischemic episodes. In the management of acute , nitrovasodilators alleviate symptoms by promoting venous capacitance and reducing pulmonary congestion, particularly in cases with elevated filling pressures. Intravenous is utilized in decompensated to enhance without significantly increasing . For hypertensive emergencies, these agents provide rapid control; , administered intravenously, is effective in severe and acute due to its balanced arterial and venous dilation. Sodium nitroprusside is further indicated for inducing controlled during surgical procedures, such as , to minimize blood loss by maintaining at targeted levels. Off-label applications include topical for anal fissures, where it relaxes the to promote healing, though this use has been partially superseded by other therapies. Historically, was explored for via nitric oxide-mediated , but it has been largely replaced by phosphodiesterase-5 inhibitors. Emerging evidence supports their potential in , particularly inhaled formulations to selectively reduce without systemic effects. As of September 2025, nebulized has shown efficacy in managing persistent of the newborn (PPHN) in neonates.

Routes of Administration

Nitrovasodilators are administered through multiple routes to achieve varying onset times and durations of action, tailored to clinical needs such as rapid relief or sustained . The sublingual and oral routes are commonly used for and derivatives. Sublingual tablets (0.3–0.6 mg) provide rapid onset within 1–3 minutes, with peak effects in 5 minutes and duration of approximately 30 minutes, making them suitable for acute scenarios like attacks. In contrast, oral (10–40 mg, three times daily) has a slower onset of 15–30 minutes and duration of 4–6 hours, ideal for prophylactic management. Transdermal and topical formulations offer sustained release for longer-term control. transdermal patches (0.2–0.8 mg/hour) or 2% ointments are applied to the skin, with onset in 5–10 minutes for ointments but typically 30–60 minutes for patches to reach , providing effects over 12–14 hours when worn daily. These are particularly suited for chronic conditions requiring consistent without frequent dosing. Intravenous administration allows for precise titration in critical settings. is given as a continuous IV (0.5–10 mcg/kg/min), with rapid onset within 2 minutes and effects lasting about 10 minutes after discontinuation, enabling fine-tuned control in intensive care environments. Similarly, IV infusions (starting at 5 mcg/min) achieve immediate onset for acute hemodynamic management. Other routes, such as buccal or inhaled forms, are employed for specific rapid-onset requirements. Buccal tablets dissolve between the cheek and gum, offering onset similar to sublingual (1–3 minutes) with duration up to 3 hours. Inhaled aerosols provide quick absorption for targeted in select cases. Pharmacokinetic variations across routes influence and , as detailed in the section.

Pharmacology

Mechanism of Action

Nitrovasodilators, such as organic nitrates, exert their vasodilatory effects through bioactivation to (NO), a key signaling molecule. This process involves the enzymatic denitration of the nitrate group by mitochondrial aldehyde dehydrogenase 2 (), which serves as a high-affinity reductase converting the parent compound into bioactive NO and reactive intermediates. The simplified bioactivation can be represented as: Nitrate→NO+reactive intermediates\text{Nitrate} \rightarrow \text{NO} + \text{reactive intermediates} This reaction occurs primarily within vascular smooth muscle cells, independent of endothelial involvement. Once released, NO diffuses into the cytosol of smooth muscle cells and binds to the heme moiety of soluble guanylate cyclase (sGC), activating the enzyme to catalyze the conversion of guanosine triphosphate (GTP) to cyclic guanosine monophosphate (cGMP). Elevated cGMP levels then activate protein kinase G (PKG), which phosphorylates downstream targets, including the inhibition of myosin light chain kinase and activation of myosin light chain phosphatase. This leads to dephosphorylation of myosin light chain, reducing actin-myosin interactions and promoting smooth muscle relaxation. The net result is vasodilation, which reduces vascular tone and preload in the cardiovascular system. The vasodilatory action of nitrovasodilators demonstrates vascular selectivity based on dose. At low doses, they preferentially dilate veins, decreasing venous return and cardiac preload with minimal effects on arterial resistance. At higher doses, arterial dilation becomes more prominent, lowering systemic and . This endothelium-independent mechanism distinguishes nitrovasodilators from endogenous NO pathways, allowing direct relaxation of vascular even in the presence of .

Pharmacokinetics

Nitrovasodilators, particularly organic nitrates such as and , undergo extensive first-pass in the liver following , resulting in low systemic . For example, oral exhibits an average of approximately 25%, with significant interindividual variability (10% to 90%) attributable to hepatic presystemic extraction. This effect is largely avoided with sublingual or intravenous routes, which enable rapid absorption and higher plasma concentrations; sublingual , for instance, achieves about 40% , influenced by mucosal and patient hydration status. Metabolism of these agents primarily involves hepatic enzymatic reduction to , the key bioactive species, often via denitration processes. vary considerably across nitrovasodilators, reflecting differences in metabolic stability: displays a brief plasma of 1 to 4 minutes owing to rapid extrahepatic and hepatic denitration, whereas has a of around 1 hour, with its pharmacologically isosorbide-5-mononitrate persisting for 4 to 6 hours. Agent-specific metabolic pathways contribute to clinical variability. is swiftly converted to dinitrate and mononitrate metabolites through mitochondrial aldehyde dehydrogenase-mediated processes. In contrast, , an inorganic nitrovasodilator administered intravenously, decomposes non-enzymatically to release while generating ions that bind , forming cyanmethemoglobin; subsequent conversion to requires monitoring to prevent toxicity during extended infusions. Excretion of nitrovasodilator metabolites occurs predominantly via the renal route. Denitrated products from organic nitrates, such as glyceryl mononitrates and isosorbide mononitrates, are cleared in urine, while thiocyanate from sodium nitroprusside elimination can accumulate in renal impairment, prolonging its half-life to 6 to 9 days.

Safety Profile

Contraindications

Nitrovasodilators, such as nitroglycerin and sodium nitroprusside, carry absolute contraindications in conditions where their vasodilatory effects could critically impair hemodynamics and organ perfusion. Severe hypotension, defined as systolic blood pressure below 90 mm Hg or a drop greater than 30 mm Hg from baseline, is an absolute contraindication, as these agents exacerbate the condition by further reducing vascular resistance and preload. Cardiogenic shock represents another absolute contraindication, where nitrovasodilators should neither be initiated nor continued, as they can worsen cardiac output and lead to multiorgan failure. Right ventricular infarction is contraindicated due to the preload dependence of the right ventricle; venodilation reduces venous return, potentially causing profound hypotension and decreased left ventricular filling. Similarly, hypertrophic cardiomyopathy with left ventricular outflow tract obstruction is an absolute contraindication, as vasodilation may increase the dynamic obstruction and impair cardiac performance. Relative contraindications apply in scenarios where benefits may outweigh risks but require heightened vigilance and potential dose adjustments. Recent use of phosphodiesterase-5 (PDE5) inhibitors, such as (within 24 hours) or (within 48 hours), is a relative due to synergistic enhancement of , resulting in severe, potentially life-threatening . Severe is also relative, as the reduced oxygen-carrying capacity of blood can be further compromised by vasodilation-induced , limiting tissue oxygenation. In special populations, nitrovasodilators demand caution in , where uncorrected low intravascular volume heightens the risk of excessive ; fluid resuscitation is typically required beforehand. Concurrent administration with other vasodilators, such as or alpha-blockers, necessitates careful monitoring to mitigate additive hypotensive effects that could precipitate adverse outcomes. Use in is classified as Category C by the FDA, with potential risks of maternal leading to fetal hypoxia; benefits must outweigh risks, and monitoring is essential. In , caution is advised, particularly with in neonates due to heightened toxicity risk; dosing adjustments and close monitoring are required. These precautions primarily aim to avert severe hypotensive episodes, as detailed in the adverse effects section.

Adverse Effects

Nitrovasodilators, such as organic nitrates and , commonly cause side effects related to their vasodilatory properties, including due to cerebral , flushing, , and reflex . These effects arise from nitric oxide-mediated relaxation, leading to peripheral and compensatory increases. Serious adverse effects include , which can result in syncope and falls, particularly in patients with preload-dependent conditions. High-dose intravenous may induce , characterized by reduced oxygen-carrying capacity of , presenting with , fatigue, and despite normal PaO2; this is rare but requires prompt treatment with . carries a risk of toxicity, especially with prolonged infusions exceeding 48 hours, high doses, or in patients with renal or hepatic impairment, manifesting as , altered mental status, seizures, and cardiovascular collapse. Many adverse effects are dose-dependent, stemming from venous pooling that reduces cardiac preload and contributes to and . Additionally, chronic use can lead to tolerance-related reduced efficacy, limiting therapeutic benefits over time.

Drug Interactions

Nitrovasodilators, such as and , exhibit significant interactions with phosphodiesterase type 5 (PDE5) inhibitors like , , and , which are contraindicated due to potentiation of hypotensive effects through increased (cGMP) levels, potentially leading to severe , syncope, or myocardial ischemia. This interaction arises because nitrovasodilators release to activate and elevate cGMP, while PDE5 inhibitors prevent cGMP degradation, amplifying beyond compensatory mechanisms. Concurrent use with other antihypertensives or vasodilators, including alpha-blockers and direct-acting agents like , results in additive hypotensive effects due to synergistic reduction in systemic and preload. Similarly, combinations with , such as amlodipine or verapamil, can cause marked and symptomatic drops, necessitating careful monitoring and dose adjustments. N-acetylcysteine (NAC) enhances the vasodilatory efficacy of nitrovasodilators by providing sulfhydryl groups that facilitate release and bioavailability, potentially improving hemodynamic responses in conditions like or , though it may also increase side effects such as . Alcohol consumption exacerbates with nitrovasodilators by additively impairing vascular tone and autonomic reflexes, heightening risks of and syncope. Beta-blockers, such as metoprolol or , when co-administered with nitrovasodilators, may mask reflex induced by venodilation, potentially leading to unopposed without the usual compensation, though their combined use is often beneficial for management.

Nitrate Tolerance

tolerance refers to the progressive loss of vasodilatory and anti-ischemic effects of nitrovasodilators, such as (GTN), following continuous or frequent exposure, limiting their long-term efficacy in conditions like . This phenomenon includes rapid tolerance, which develops within hours of high-dose administration and manifests as acute to hemodynamic responses, and , where desensitization extends to other organic nitrates (e.g., ) and endothelium-derived pathways. The primary mechanisms involve intracellular changes that impair (NO) bioavailability and signaling. Depletion of sulfhydryl groups, particularly through oxidative modification of mitochondrial aldehyde dehydrogenase-2 (), reduces the enzyme's activity in bioconverting nitrates to bioactive NO, leading to diminished . Concurrently, nitrate exposure induces by elevating production via activation and mitochondrial generation, which scavenges NO to form , further inhibiting soluble (sGC) and exacerbating tolerance. Prevention strategies center on interrupting continuous exposure to allow vascular recovery. Implementing nitrate-free intervals of 10-12 hours daily, such as overnight from patches, effectively restores responsiveness by enabling replenishment of sulfhydryl donors and reduction of . Adjunctive antioxidants like have shown potential in preclinical models to mitigate superoxide-mediated NO scavenging, though clinical evidence remains limited and inconsistent. Dose adjustments, including eccentric dosing regimens, can also help maintain efficacy without full tolerance development. Clinically, nitrate tolerance results in attenuated anti-anginal efficacy, with reduced relief of and hemodynamic benefits after prolonged , potentially increasing ischemic events and necessitating alternative treatments.

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