BRIEF COMMUNICATIONS Acetylcholine Release from Rat Atria Can Be Regulated through an arAdrenergic Receptor

Isolated superfused rat atria release [H]acetylcholine when depolarized with 57 mM potassium. The depolarization-induced overflow of [H]acetylcholine is markedly inhibited by micromolar concentrations of epinephrine and norepinephrine. The a,-selective adrenergic agonist methoxamine also inhibits tritium overflow, but the «2-selective adrenergic agonist clonidine and the 0-adrenergic agonist isoproterenol do not. Prazosin, an selective «i-adrenergic antagonist, blocks adrenergic inhibition of [H]acetylcholine overflow with a K, of approximately 0.4 nM. Yohimbine has approximately one-hundredth the potency of prazosin for blocking adrenergic inhibition of [H]acetylcholine overflow. [H]Norepinephrine overflow from isolated rat atria is also inhibited by norepinephrine, but this effect is antagonized by yohimbine and not by prazosin. We suggest that the release of acetylcholine from cardiac parasympathetic neurons can be regulated through an «i -adrenergic receptor, and that this mechanism may underly, at least in part, the relative lack of effects of prazosin on heart rate. (Circ Res 56: 763-766, 1985)