Betaadrenergic

Beta-adrenergic refers to a class of adrenergic receptors that respond to catecholamines epinephrine and norepinephrine. The beta-adrenergic receptors (β-ARs) are seven transmembrane G protein-coupled receptors that, upon activation, stimulate adenylate cyclase via the Gs protein, increasing intracellular cyclic AMP (cAMP).

There are three main subtypes: beta-1 (β1), beta-2 (β2), and beta-3 (β3). In humans, β1 receptors are primarily in the heart and to a lesser extent in juxtaglomerular cells; β2 receptors are abundant in smooth muscle of the airways and vasculature; β3 receptors are prominent in adipose tissue and also found in the bladder and some smooth muscles.

Activation of β1 increases heart rate and contractility, and can stimulate renin release. β2 promotes bronchodilation, vasodilation in skeletal muscle, and metabolic effects such as glycogenolysis and lipolysis. β3 influences lipolysis and thermogenesis. The net cardiovascular and metabolic responses depend on receptor distribution and the balance of receptor subtype activation.

Pharmacology: beta-adrenergic agonists mimic sympathetic stimulation; non-selective agonists include isoproterenol; beta-1 selective agonists include dobutamine; beta-2 selective agonists include terbutaline and salbutamol. Antagonists (beta blockers) include non-selective propranolol and cardioselective agents such as metoprolol, atenolol. These agents are used to treat hypertension, angina, arrhythmias, heart failure, and asthma/COPD with varying receptor selectivity and side effects.

Understanding beta-adrenergic signaling is central to physiology and pharmacology, linking autonomic control to cardiovascular, respiratory, and metabolic systems. Dysregulation or pharmacologic blockade can contribute to disease management and adverse effects, such as bronchospasm from beta-blockade or bronchoconstriction from excessive sympathetic activity.