Endothelin-1 and insulin activate the steady-state voltage dependent R-type Ca2+ channel in aortic smooth muscle cells via a pertussis toxin and cholera toxin sensitive G-protein |
| |
Authors: | Bkaily Ghassan Naik Radha Jaalouk Doris Jacques Danielle Economos Demetri D'Orléans-Juste Pédro Pothier Pierre |
| |
Institution: | (1) MRCC Group on Immuno-Cardiovascular Interaction, Department of Anatomy and Cell Biology, Faculty of Medicine, Université de Sherbrooke, Sherbrooke, Québec, J1H 5N4, Canada;(2) Department of Pharmacology, Faculty of Medicine, Université de Sherbrooke, Sherbrooke, Québec, J1H 5N4, Canada |
| |
Abstract: | In single rabbit aortic smooth muscle cells, and at a concentration known to induce a maximum sustained increase of intracellular Ca2+ via activation of the steady-state voltage dependent R-type Ca2+ channels, endothelin-1 (10-7 M) and insulin (80 U/ml) were found to induce a sustained increase in cytosolic free Ca2+ (Ca]i) levels that was significantly attenuated by pre-treatment with either pertussis toxin (PTX), cholera toxin (CTX) or removal of extracellular Ca2+.However, both PTX and CTX failed to inhibit the sustained depolarization-evoked sustained Ca2+ influx and Ca]i elevation via activation of the R-type Ca2+ channels. Moreover, ET-1 and insulin-evoked sustained increases in Ca2+ influx were not attenuated by the selective PKC inhibitor, bisindolylmaleimide (BIS), or the specific L-type Ca2+ channel blocker, nifedipine, but were completely reversed by the R-type Ca2+ channel blocker, (-) PN 200-110 (isradipine). These data suggest that both insulin and ET-1 activate the nifedipine-insensitive but isradipine-sensitive steady state voltage dependent R-type Ca2+ channels present on rabbit VSMCs and these channels are directly coupled to PTX and CTX sensitive G protein(s). |
| |
Keywords: | aortic cells steady state R-type Ca2+ channel ET-1 insulin calcium G-protein |
本文献已被 SpringerLink 等数据库收录! |
|