INDUCTION OF CA++ INFLUX AND INTRACELLULAR CA++ RELEASE IN ISOLATED RAT AORTA AND MESENTERIC RESISTANCE VESSELS BY NOREPINEPHRINE ACTIVATION OF ALPHA-1 RECEPTORS

Abstract

Which .alpha. adrenoceptor subtypes(s) is involved in the activation of isolated rat aorta and mesenteric resistance vessels by norepinephrine was studied, and whether norepinephrine-incuded Ca2+ influx into the smooth muscle is activated by 1 .alpha. adrenoceptor subtype while intracellular Ca2+ release is mediated by the other subtype was ascertained. The concentration-response curves for prazosin and yohimbine inhibition of norepinephrine-induced 45Ca influx, intracellular Ca2+ release (as judged from contractions in Ca2+-free solution) and contraction in the rat aorta indicate that the norepinephrine activation of the .alpha.-1 adrenoceptor was responsible for both Ca2+ mobilization processes leading to norepinephrine contraction of this tissue. Contractions induced by norepinephrine in the isolated rat mesenteric resistance vessels demonstrated a phasic component, which was primarily dependent on intracellular Ca2+ release, and a tonic component, which was completely dependent on Ca2+ influx. Prazosin was 3 orders of magnitude more potent than yohimbine in inhibiting both components of the norepinephrine contracture in these vessels. Norepinephrine activation of .alpha.-1 adrenoceptors is responsible for both Ca2+ influx and intracellular Ca2+ release in isolated rat aorta and mesenteric resistance vessels.