Cardioselectivity is dose-dependent: β 2 receptor blocking activity increases with higher doses.

Nebivolol is the only beta blocker that causes NO-mediated vasodilation: it decreases vascular resistance by stimulating β 3 receptors and activating NO synthase in the vasculature.

Decrease the heart rate, contractility, and AVN conductivity.

Selectively bind to and block β 1 receptors, which are primarily found in the heart.

With intrinsic sympathomimetic activity ( ISA) OverviewĬardioselective beta blockers ( β 1 selective) Initiation and cessation of beta-blocker therapy should always be gradual to avoid side effects or symptoms of withdrawal (e.g., rebound tachycardia, hypertension, acute cardiac death).

Beta blockers are contraindicated in patients with symptomatic bradycardia, AV block, decompensated heart failure, and asthma. Propranolol, a nonselective beta blocker, is the first-line drug in the management of essential tremor, portal hypertension, migraine prophylaxis, and thyroid storm. Cardioselective beta blockers have a lower side-effect profile and are preferred in the management of coronary heart disease, compensated heart failure, acute coronary syndrome, and certain types of arrhythmias. Nonselective beta blockers (e.g., pindolol, propranolol) inhibit all β receptors and may cause bronchoconstriction, peripheral vasoconstriction, and metabolic imbalances (e.g., hypoglycemia and hyperglycemia, hypertriglyceridemia) in addition to cardiac effects.

Cardioselective blockers (e.g., atenolol, bisoprolol) primarily block β 1 receptors in the heart, causing decreased heart rate, cardiac contractility, cardiac workload, and AVN conduction. Beta blockers are a group of drugs that inhibit the sympathetic activation of β-adrenergic receptors.

Antidote for beta blocker overdose