Adrenergic modulation of vascular prostacyclin (PGI₂) secretion

An in vitro model for the study of adrenoreceptor-prostacyclin (PGI₂) relationships in the rat aorta is described. PGI₂ synthesis was stimulated by adrenergic agonists (rank order of potency: epinephrine > norepinephrine > phenylephrine > methoxamine). Isoproterenol, UK 14304, clonidine and salbutamol were without effect. Epinephrine (3 × 10^-7 M)-stimulated PGI₂ synthesis was inhibited by adrenoreceptor antagonists (rank order of potency: yohimbine > prazosin > phentolamine > corynanthine ≫ propranolol). The absence of calcium in incubation media abolished epinephrine-stimulated PGI₂ synthesis as did the calcium channel blocker, verapamil, in a dose-dependent manner. Calcium ionophore A23187 (10^-5 M)-stimulated as inhibited by verapamil (in a dose-dependent manner), but not by prazosin, phentolamine or yohimbine. It is concluded that epinephrine-mediated rat aortic PGI₂ synthesis is α-adrenoceptor- and not β-adrenoceptor-mediated, calcium-dependent, and that the α-adrenoceptor antagonists evaluated do not have verapamil-like calcium channel blocking activities. These findings may be relevant to contraction-relaxation cycles of vascular tissue.