Adrenergic modulation of vascular prostacyclin (PGI2) secretion

Abstract

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 greater than norepinephrine greater than phenylephrine greater than methoxamine). Isoproterenol, UK 14304, clonidine and salbutamol were without effect. Epinephrine (3 X 10(-7) M)-stimulated PGI2 synthesis was inhibited by adrenoreceptor antagonists (rank order of potency: yohimbine greater than prazosin greater than phentolamine greater than corynanthine much greater than 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 PGI2 synthesis was 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 alpha-adrenoceptor- and not beta-adrenoceptor-mediated, calcium-dependent, and that the alpha-adrenoceptor antagonists evaluated do not have verapamil-like calcium channel blocking activities. These findings may be relevant to contraction-relaxation cycles of vascular tissue.