Vasodilators

Vasodilators are drugs that widen blood vessels by relaxing vascular smooth muscle. They reduce vascular resistance and can affect arteries, veins, or both. Vasodilation can be endothelium-dependent, often involving nitric oxide signaling and cyclic GMP, or endothelium-independent, through direct action on smooth muscle cells or changes in intracellular calcium.

Pharmacologic vasodilators are used to treat hypertension, heart failure, angina, and pulmonary arterial hypertension; some are used for erectile dysfunction in combination with other agents. They can be categorized by their primary vascular targets and mechanisms. Nitrate and nitrite donors (such as nitroglycerin and isosorbide dinitrate) primarily cause venodilation, reducing preload. Arterial dilators (for example hydralazine, minoxidil) decrease afterload, while agents like diazoxide act on arterioles. Nitroprusside is a potent dilator of both arteries and veins. Calcium channel blockers (amlodipine, nifedipine; diltiazem, verapamil) relax vascular smooth muscle by inhibiting calcium influx. Inhibitors of the renin–angiotensin system (ACE inhibitors like enalapril and ARBs like losartan) produce vasodilation by reducing angiotensin II–mediated constriction and, for ACE inhibitors, by increasing bradykinin. For pulmonary arterial hypertension, prostacyclin analogs (epoprostenol, treprostinil), endothelin receptor antagonists (bosentan, ambrisentan), and PDE-5 inhibitors (sildenafil, tadalafil) are used to promote pulmonary vasodilation.

Adverse effects commonly include headache, flushing, edema, dizziness, and hypotension; reflex tachycardia can occur with some agents. Drug interactions—such as those between nitrates and PDE-5 inhibitors—require careful management.