Induction of Ca++ influx and intracellular Ca++ release in isolated rat aorta and mesenteric resistance vessels by norepinephrine activation of alpha-1 receptors.

This study was undertaken to determine which alpha adrenoceptor subtype(s) is involved in the activation of isolated rat aorta and mesenteric resistance vessels by norepinephrine and to ascertain whether norepinephrine-induced Ca++ influx into the smooth muscle is activated by one alpha adrenoceptor subtype while intracellular Ca++ release is mediated by the other subtype. The concentration-response curves for prazosin and yohimbine inhibition of norepinephrine-induced 45Ca influx, intracellular Ca++ release (as judged from contractions in Ca++-free solution) and contraction in the rat aorta indicate that the norepinephrine activation of the alpha-1 adrenoceptor was responsible for both Ca++ 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 shown to be primarily dependent on intracellular Ca++ release, and a tonic component, which was completely dependent on Ca++ influx. Prazosin was three orders of magnitude more potent than yohimbine in inhibiting both components of the norepinephrine contracture in these vessels. We conclude that norepinephrine activation of alpha-1 adrenoceptors is responsible for both Ca++ influx and intracellular Ca++ release in isolated rat aorta and mesenteric resistance vessels.