Category: receptor_pharmacology
Catecholamine GPCRs split into α-family (Gq-coupled vasoconstriction at α1; Gi-coupled presynaptic feedback inhibition at α2) and β-family (Gs-coupled cAMP elevation: β1 cardiac chronotropy + inotropy, β2 bronchodilation + vasodilation, β3 lipolysis + detrusor relaxation). Antagonists branch by subtype: non-selective β-blockers (propranolol, nadolol, sotalol) block β1+β2; β1-cardioselective (atenolol, metoprolol, bisoprolol) preserve bronchodilation at therapeutic doses; mixed α/β (carvedilol, labetalol) add vasodilation. α1-blockers (prazosin, doxazosin, tamsulosin) lower BP + relax urethra. α2-agonists (clonidine, guanfacine) suppress central sympathetic outflow. β2-agonists (albuterol, salmeterol) relax bronchial smooth muscle. Sympathomimetics (ephedrine, pseudoephedrine, phenylephrine, synephrine) activate α + β to varying degrees. NRI (atomoxetine) blocks NET, raising synaptic NE without the abuse potential of stimulants.