Activation of calcium sparks by angiotensin II in vascular myocytes.

Serge Arnaudeau, Nathalie Macrez-Leprêtre, Jean Mironneau
Biochemical and Biophysical Research Communications. 1996-05-01; 222(3): 809-815
DOI: 10.1006/bbrc.1996.0808

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1. Biochem Biophys Res Commun. 1996 May 24;222(3):809-15.

Activation of calcium sparks by angiotensin II in vascular myocytes.

Arnaudeau S(1), Macrez-Leprêtre N, Mironneau J.

Author information:
(1)Laboratoire de Physiologie Cellulaire et Pharmacologie Moléculaire, CNRS ESA
5017, Université de Bordeaux II, France.

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 (InsP3) generation induced by various mediators
and involved InsP3-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
AT1 receptors stimulate Ca2+ sparks through activation of L-type Ca2+ channels
without involving InsP3-induced Ca2+ release. This novel transduction pathway may
be a common mechanism for vasoconstrictors which do not stimulate generation of
chemical second messengers.

DOI: 10.1006/bbrc.1996.0808
PMID: 8651927 [Indexed for MEDLINE]

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