Autor: |
Higa T; Department of Cellular Pharmacology, Hokkaido University Graduate School of Medicine, Sapporo, Japan., Horinouchi T, Aoyagi H, Asano H, Nishiya T, Nishimoto A, Muramatsu I, Miwa S |
Jazyk: |
angličtina |
Zdroj: |
Journal of pharmacological sciences [J Pharmacol Sci] 2010; Vol. 113 (3), pp. 276-80. Date of Electronic Publication: 2010 Jun 29. |
DOI: |
10.1254/jphs.10102sc |
Abstrakt: |
The mechanism for sustained Ca2+ influx activated by G protein-coupled receptors was examined. In Chinese hamster ovary cells expressing recombinant human endothelin type B receptor (ET(B)R) and endogenous P2Y receptor (P2Y-R), endothelin-1 elicited a sustained Ca2+ influx depending on G(q/11 )protein, phospholipase C (PLC), Na+/H+ exchanger (NHE), and p38 mitogen-activated protein kinase (p38MAPK), whereas P2Y-R-induced sustained Ca2+ influx was negligible. Functional studies showed that NHE activation by ET(B)R was mediated via p38MAPK but not G(q/11)/PLC, while that by P2Y-R involves only G(q/11)/PLC/p38MAPK. These results suggest that G(q/11)/PLC-independent NHE activation via p38MAPK plays an important role in ET(B)R- mediated sustained Ca2+ influx. |
Databáze: |
MEDLINE |
Externí odkaz: |
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