Non-genomic mechanism of corticosterone inhibition of bradykinin-induced calcium influx in PC12 cells: Involvement of protein kinase C

Q. Jian, W. Chenguang, H. Xiuying, L. Shujie, C. Yizhang

Research output: Contribution to journalArticle

1 Scopus citations

Abstract

Bradykinin (BK) induces an increase in [Ca2+]1 via intracellular Ca2+ release and extracellular Ca2+ influx through the transduction of G protein, but not through voltaged-sensitive calcium channels, the actions of BK can be rapidly inhibited by corticosterone (B). In this experiment. We analysed how B influences bradykinin (BK)-induced intracellular Ca2+ release and extracellular Ca2+ influx, and further studied the mechanism of the rapid action of corticosterone. To dissociate the intracellular Ca2+ release and extracellular Ca2+ influx induced by BK, the Ca2+- free/Ca2+-reintroduction protocol was used. The results were as follows: (1) The Ca2+ influx induced by BK could be rapidly inhibited by B, but intracellular Ca2+ release could not be affected significantly. (2) The inhibitory effect of B-BSA (bovine serum albumin-conjugated corticosterone) on Ca2+ influx induced by BK was the same as the effect of free B. (3) PKC activator (PMA) could mimic and PKC inhibitor Go6976 could reverse the inhibitory effect of B. (4) There was no inhibitory effect of B on Ca2+ influx induced by BK when pretreated with PTX. The results suggested that B might act via its putative membrane receptor and inhibit the Ca2+ influx induced by BK through the PTX-sensitive G protein-PKC pathway.

Original languageEnglish (US)
Pages (from-to)221-226
Number of pages6
JournalChinese Journal of Neuroscience
Volume14
Issue number4
StatePublished - Dec 1 1998

Keywords

  • Bradykinin
  • Ca
  • Corticosterone nongenomic
  • G protein
  • PC12 cells
  • PKC

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology

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