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🔬 Mechanism of Action Alpha-adrenoceptor blockers: Block α₁-receptors in vascular smooth muscle → vasodilation → ↓ peripheral resistance → ↓ blood pressure. Beta-adrenoceptor blockers: Block β₁-receptors in the heart → ↓ heart rate and contractility; also reduce renin release from the kidney → ↓ RAAS activity. Dual α/β blockers: Combine both effects, lowering blood pressure through vasodilation and reduced cardiac output. 🧩 Major Classes and Examples Class Examples Primary Effects Clinical Uses Alpha-1 blockers Prazosin, Terazosin, Doxazosin Vasodilation, ↓ BP, improve urinary flow (BPH) Hypertension, benign prostatic hyperplasia Beta-1 selective blockers Atenolol, Metoprolol, Bisoprolol ↓ HR, ↓ contractility, ↓ renin Hypertension, angina, arrhythmias, heart failure Non-selective beta blockers Propranolol, Nadolol, Timolol Block β₁ and β₂ → ↓ HR, bronchoconstriction risk Hypertension, migraine prophylaxis, portal hypertension Dual α/β blockers Labetalol, Carvedilol Vasodilation + ↓ HR/contractility Hypertension (including pregnancy), heart failure, hypertensive emergencies ⚠️ Key Considerations Alpha blockers: Risk of postural hypotension (“first-dose phenomenon”), dizziness. Beta blockers: Contraindicated in asthma/COPD (non-selective), may cause bradycardia, fatigue. Dual blockers: Useful in hypertensive emergencies and in patients with both hypertension and heart failure. Combination therapy: Often used with diuretics, ACE inhibitors, or calcium channel blockers for better BP control #hypertension