Endothelin type B receptor-induced sustained Ca2+ influx involves G(q/11)/phospholipase C-independent, p38 mitogen-activated protein kinase-dependent activation of Na+/H+ exchanger.

نویسندگان

  • Tsunaki Higa
  • Takahiro Horinouchi
  • Hiroyuki Aoyagi
  • Hiroshi Asano
  • Tadashi Nishiya
  • Arata Nishimoto
  • Ikunobu Muramatsu
  • Soichi Miwa
چکیده

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.

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عنوان ژورنال:
  • Journal of pharmacological sciences

دوره 113 3  شماره 

صفحات  -

تاریخ انتشار 2010