Adrenergic Blockers

Adrenergic blockers are competitive antagonists: they occupy adrenergic receptors without producing the sympathetic response. The clinical effect depends on which receptor is blocked. Blocking beta-1 receptors in the heart slows the sinus rate, reduces contractility, slows AV-nodal conduction, and decreases renin release from the kidney. Those effects can lower myocardial oxygen demand and ventricular rate, but they can also produce bradycardia, hypotension, fatigue, or worsening heart failure when introduced too quickly. Blocking beta-2 receptors removes sympathetic bronchodilation and reduces hepatic glycogenolysis. Non-selective beta-blockers such as propranolol, nadolol, sotalol, and ophthalmic timolol can therefore cause bronchospasm and can make hypoglycemia harder to recognize and correct. Cardioselectivity is relative, not absolute: metoprolol, bisoprolol, atenolol, and nebivolol become less selective as the dose rises, so respiratory risk increases with higher doses. [6][23] Blocking alpha-1 receptors relaxes arteriolar and venous smooth muscle, producing vasodilation. It also relaxes the prostate and bladder neck, improving urinary flow in benign prostatic hyperplasia (BPH). The same vasodilation that relieves obstruction or lowers pressure can cause dizziness, orthostatic hypotension, and syncope, particularly after the first dose or an upward...