Other Antihypertensives

Beyond the first-line drugs (diuretics, ACE-I/ARBs, calcium-channel blockers, beta-blockers), several other classes lower blood pressure by different routes — used as add-ons, for resistant hypertension, or specific situations. Three groups matter here, and each is best remembered by its distinctive adverse effect.

Alpha-1 blockers (the `-osin` drugs), central alpha-2 agonists (clonidine, methyldopa), and direct vasodilators (hydralazine, minoxidil, nitroprusside) each relax vessels or reduce sympathetic drive in their own way.

Alpha-1 blockers (prazosin, doxazosin, terazosin — `-osin`) block alpha-1 receptors on blood vessels, relaxing them to lower BP; they also relax the prostate/bladder neck, so they double as BPH treatment. Their signature danger is the "first-dose phenomenon" — severe orthostatic hypotension and syncope after the first dose — so the first dose is given at bedtime and started low.

Central alpha-2 agonists (clonidine, methyldopa) work in the brainstem, stimulating alpha-2 receptors that *reduce* sympathetic outflow — lowering heart rate and BP. Their catch is rebound hypertension: stopping clonidine abruptly removes the brake and causes a dangerous BP surge, so it must be tapered. (Methyldopa is a preferred antihypertensive in pregnancy.)

Direct vasodilators relax arterial smooth muscle powerfully. Because the sudden BP drop triggers a reflex sympathetic response, they cause reflex tachycardia and fluid retention (often co-prescribed with a beta-blocker and diuretic). Hydralazine can cause a drug-induced lupus-like syndrome (fever, joint pain, rash — reversible on stopping). Minoxidil causes hirsutism (its topical form treats hair loss).

Sodium nitroprusside is a potent IV vasodilator for hypertensive emergencies — but it is metabolized to cyanide, so prolonged/high-rate infusion risks cyanide toxicity (metabolic acidosis, altered mental status); it is light-protected, titrated, and time-limited.