Activation of calcium sparks by angiotensin II in vascular myocytes

Contraction in smooth muscle is triggered by an increase in cytoplasmic free calcium ([Ca2+](i)) which depends on both Ca2+ influx through L-type Ca2+ channels and Ca2+ release from the sarcoplasmic reticulum (SR). Two mechanisms have been shown to be involved in SR Ca2+ release. one is stimulated by Ca2+ and involved ryanodine-sensitive Ca2+-release channels; the other is stimulated by an increase in inositol 1,4,5-trisphosphate (InsP(3)) generation induced by various mediators and involved InsP(3)-sensitive Ca2+ release channels. Here, we examined the effects of angiotensin II on [Ca2+](i) in single rat portal vein myocytes using both the whole cell patch-clamp method and a laser scanning confocal microscope. Elementary Ca2+ release events (Ca2+ sparks) were obtained spontaneously or in response to L-type Ca2+ channel current activation, and resulted from activation of ryanodine-sensitive Ca2+-release channels in the SR. We show that angiotensin AT(1) receptors stimulate Ca2+ sparks through activation of L-type Ca2+ channels without involving InsP(3)-induced Ca2+ release. This novel transduction pathway may be a common mechanism for vasoconstrictors which do not stimulate generation of chemical second messengers. (C) 1996 Academic Press, Inc.