Topic overview

Start with the big picture

Catecholamine synthesis begins with tyrosine, and tyrosine hydroxylase catalyzes its rate-limiting conversion to DOPA. Catecholamines are stored in vesicles through VMAT, released by calcium-dependent exocytosis, and their actions are terminated mainly through norepinephrine reuptake by NET, followed by metabolism by MAO and COMT. Receptor coupling helps explain their effects: α1 receptors signal through Gq, α2 through Gi, and β receptors through Gs. These pathways underlie effects such as α1-mediated vasoconstriction, β1-related increases in heart rate and contractility, and β2-mediated bronchodilation. The topic also introduces selective and non-selective agonists, indirect-acting agents, α and β blockers, and clinically relevant adverse effects and interactions.