What is the mechanism of action of beta-blockers?

Beta-blockers function primarily by blocking beta-adrenergic receptors, which are a class of G protein-coupled receptors that mediate the effects of catecholamines (such as adrenaline and noradrenaline) in the body. By inhibiting these receptors, beta-blockers reduce the effects of sympathetic nervous system activation. This leads to a decrease in heart rate, contractility, and conduction velocity through the atrioventricular node, ultimately lowering blood pressure and oxygen demand from the heart muscle.

In the context of cardiovascular conditions, beta-blockers are used to manage hypertension, heart failure, and arrhythmias, among other indications. Their ability to mitigate stress and anxiety responses, as well as to prevent migraines, also underscores their versatility in clinical application.

The other options represent mechanisms associated with different classes of medications. Blocking calcium channels pertains to calcium channel blockers, which are used for hypertension and angina by preventing calcium entry into cardiac and smooth muscle cells. Inhibiting the angiotensin-converting enzyme relates to ACE inhibitors, which lower blood pressure by preventing the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. Enhancing the effect of acetylcholine describes anticholinesterase