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+...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 1996-05, Vol.222 (3), p.809-815
Main Authors: Arnaudeau, Serge, Macrez-Leprêtre, Nathalie, Mironneau, Jean
Format: Article
Language:English
Subjects:
Angiotensin II - pharmacology
Animals
Calcium - metabolism
Calcium Channels - metabolism
Cells, Cultured
Cellular Biology
Dihydropyridines - pharmacology
Ion Channel Gating - drug effects
Life Sciences
Membrane Potentials
Muscle, Smooth, Vascular - metabolism
Patch-Clamp Techniques
Portal Vein
Rats
Rats, Wistar
Receptors, Angiotensin - physiology
Subcellular Processes
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Summary: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+]iin 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 AT1receptors 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.
ISSN:0006-291X
1090-2104
DOI:10.1006/bbrc.1996.0808