Beta Adrenergics

Beta adrenergic medications change sympathetic signalling at beta receptors. The first clinical question is not “Which beta drug is this?” but “Is this drug stimulating or blocking which receptor, in which patient?” Beta-1 receptors predominate in the heart and juxtaglomerular apparatus. Stimulation increases heart rate, myocardial contractility, atrioventricular-node conduction, and renin release. Blocking beta-1 receptors slows the sinus rate, slows AV conduction, decreases contractility, and reduces myocardial oxygen demand. Those effects can relieve tachyarrhythmia or angina, but the same effects can cause symptomatic bradycardia, hypotension, or low cardiac output. Beta-2 receptors predominate in bronchial and vascular smooth muscle. Stimulation relaxes bronchial smooth muscle and shifts potassium from the extracellular space into cells. Beta-2 activity also contributes to hepatic glycogenolysis. This explains a recognizable cluster after repeated or high-dose beta-2 agonist treatment: tremor, palpitations, tachycardia, falling potassium, and sometimes rising glucose. Beta-2 blockade removes bronchodilation and can blunt autonomic warning symptoms of hypoglycemia. A medication may be relatively selective, but selectivity is not absolute. Metoprolol is relatively beta-1 selective at usual doses; propranolol, nadolol, and timolol block beta-1 and beta-2 receptors....