vasodepressors

Vasodepressors are a class of drugs that cause relaxation of vascular smooth muscle, leading to vasodilation and a reduction in systemic vascular resistance. They are used to lower blood pressure and to improve blood flow in conditions where constricted vessels contribute to symptoms. The term vasodepressor is often used interchangeably with vasodilator, though some sources distinguish direct vasodilators from agents that act indirectly to oppose vasoconstriction.

The mechanisms of action among vasodepressors are diverse. Some drugs, such as organic nitrates and nitroprusside, donate or enhance nitric oxide signaling, increasing cyclic GMP in smooth muscle and promoting relaxation. Calcium channel blockers reduce intracellular calcium, impairing contraction of vascular smooth muscle. Direct arteriolar dilators like hydralazine and minoxidil open potassium channels or otherwise alter smooth muscle excitability to cause dilation. Across drug classes, inhibition of the renin–angiotensin system (ACE inhibitors, ARBs) lessens angiotensin II–mediated vasoconstriction. Other agents, including alpha-1 blockers and certain dopaminergic or endothelin-pathway antagonists, produce vasodilation through receptor-mediated mechanisms. Some drugs have selective effects on the arterial or venous beds, while others produce mixed vascular effects.

Common clinical uses include treatment of hypertension, hypertensive emergencies, angina, and heart failure in selected patients. Vasodepressors are also employed in pulmonary arterial hypertension and in perioperative settings where controlled vasodilation is needed. Adverse effects frequently include hypotension, reflex tachycardia, headache, dizziness, and edema; interactions with other antihypertensives or vasodilatory drugs can amplify these effects.

In summary, vasodepressors encompass a range of agents that relieve vascular tone through varying mechanisms, with applications in cardiovascular disease and careful consideration of hemodynamic effects and risks.