Pharmacology

β1‑adrenergic receptors are predominantly located in the heart; blockade reduces heart rate and contractility, decreasing cardiac output. β2 receptors mediate bronchial smooth muscle relaxation and vasodilation, so a selective β1 blocker spares these functions, avoiding bronchoconstriction and peripheral vasodilation. Renin release is mediated by β1 receptors, so blockade actually reduces renin.

Aminoglycosides exhibit concentration-dependent killing, meaning their bactericidal efficacy increases as the peak drug concentration rises above the minimum inhibitory concentration. In contrast, beta-lactams demonstrate time-dependent killing, where the duration of drug exposure above the MIC is the critical determinant of efficacy.

Beta-blockers reduce blood pressure primarily by antagonizing beta-1 adrenergic receptors, which decreases heart rate and myocardial contractility, thereby lowering cardiac output. A diagram for this topic isn't available yet — the worked example below walks the same reasoning step by step.

• !They do not block angiotensin II receptors directly; that is the mechanism of angiotensin receptor blockers (ARBs).

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