Is metoprolol (beta-1 blocker) more selective than sotalol (nonselective beta-blocker)?

Metoprolol vs Sotalol: Beta-Receptor Selectivity

Metoprolol is a beta-1 selective (cardioselective) blocker, while sotalol is a nonselective beta-blocker that blocks both beta-1 and beta-2 receptors equally. 1, 2

Key Pharmacologic Differences

Metoprolol (Beta-1 Selective)

• Metoprolol preferentially blocks beta-1 adrenergic receptors located primarily in the myocardium, though this selectivity is not absolute at higher plasma concentrations. 1
• At higher doses, metoprolol also inhibits beta-2 adrenoreceptors in bronchial and vascular smooth muscle, but requires higher concentrations to do so compared to beta-1 blockade. 1, 3
• In asthmatic patients, metoprolol reduces FEV1 and FVC significantly less than nonselective beta-blockers like propranolol at equivalent beta-1 receptor blocking doses. 1
• Metoprolol cannot reverse the beta-2-mediated vasodilating effects of epinephrine in healthy subjects, demonstrating its relative beta-1 selectivity. 1

Sotalol (Nonselective)

• Sotalol is a competitive beta-adrenoceptor antagonist with no preferential actions on beta-1 or beta-2 responses, blocking both receptor types equally. 2
• Sotalol blocks all beta-receptor-mediated responses without cardioselectivity. 4
• In addition to nonselective beta-blockade (Class II effect), sotalol has Class III antiarrhythmic activity that prolongs action potential duration and repolarization. 2

Clinical Implications of Selectivity

Respiratory Considerations

• Patients with classical pulmonary asthma may worsen their condition with nonselective beta-blockers like sotalol or agents with low beta-1 selectivity. 5
• Cardioselective beta-blockers like metoprolol do not affect the action of bronchodilators but reduce the heart rate acceleration caused by their use. 5
• When patients with mild wheezing or COPD require beta-blockade, low doses of a beta-1 selective agent like metoprolol (12.5 mg) should be used rather than complete avoidance. 5

Cardiovascular Effects

• Both agents reduce heart rate, cardiac output, and systolic blood pressure, but through different receptor mechanisms. 1, 2
• Sotalol's nonselective blockade causes concentration-dependent increases in contractility unrelated to beta-blockade, possibly due to inhibition of time-dependent potassium current. 2
• Sotalol has occasional proarrhythmic effects that limit its use, particularly noted in hypertension management. 5

Metabolic Considerations

• Nonselective beta-blockers like sotalol are associated with lower HDL cholesterol, increased triglycerides, and may cause type-2 diabetes. 5
• Nonselective agents may be preferable in some situations to antagonize beta-2-mediated metabolic effects such as epinephrine-induced hypokalemia. 3

Common Pitfalls

The most critical error is assuming metoprolol's beta-1 selectivity is absolute—at higher doses, it loses cardioselectivity and blocks beta-2 receptors. 1, 3 This means that even "selective" agents can cause bronchospasm, peripheral vasoconstriction, and metabolic effects when dosed aggressively.

Another pitfall is using sotalol without considering its proarrhythmic potential, which is unrelated to its nonselective beta-blockade but stems from its Class III effects. 5, 2

For patients requiring beta-blockade with pulmonary disease, male impotency concerns, or metabolic syndrome, metoprolol's beta-1 selectivity offers meaningful clinical advantages over sotalol's nonselective blockade. 5