Adrenergic Agonists

Adrenergic agonists activate receptors normally stimulated by norepinephrine and epinephrine. The receptor profile—not the broad label “sympathomimetic”—predicts what the patient will experience. | Receptor | Main physiologic effect | Bedside consequence | |---|---|---| | Alpha-1 | Arteriolar and venous vasoconstriction | Increased systemic vascular resistance and blood pressure; reduced mucosal oedema; excessive stimulation can impair tissue perfusion | | Alpha-2 | Reduced central sympathetic outflow | Lower blood pressure and often a slower heart rate; abrupt withdrawal can produce rebound hypertension | | Beta-1 | Increased sinoatrial rate and myocardial contractility | Increased cardiac output, myocardial oxygen demand, and risk of tachyarrhythmia | | Beta-2 | Bronchial smooth-muscle relaxation; potassium movement into cells | Bronchodilation, tremor, tachycardia, and possible hypokalaemia | | Dopaminergic receptors | Agent- and dose-dependent vascular and cardiac effects | The clinical effect depends on the drug, dose, patient state, and competing receptor activity | A few examples make the pattern easier to use. Epinephrine activates alpha- and beta-receptors, which is why it can reverse both vasodilatory shock and bronchospasm in anaphylaxis. Norepinephrine is predominantly an alpha-1...