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Carbachol but not bradykinin blocks the enkephalin-induced calcium transient in human neuroblastoma SK-N-SH cells.

作者信息

Liu T Y, Chueh S H

机构信息

Department of Biochemistry, National Defense Medical Center, Taipei, Taiwan, ROC.

出版信息

Chin J Physiol. 1995;38(2):75-80.

PMID:8697901
Abstract

Carbachol stimulated significantly higher increase in inositol 1,4,5-trisphosphate (IP3) generation than did leucine-enkephalin (leu-EK) and bradykinin in SK-N-SH cells. When leu-EK was concomitantly added with carbachol, an additive effect was observed in IP3 generation. However, the rise in cytosolic Ca2+ concentration ([Ca2+]i) reached the same level as that induced by carbachol alone. On the other hand, additive effects were observed in both [Ca2+]i rise and IP3 generation when leu-EK was simultaneously added with bradykinin. Furthermore, cells lost their [Ca2+]i response to leu-EK if carbachol was first added to induce a [Ca2+]i increase whereas the response was unchanged if leu-EK was added after addition of bradykinin. Our results suggest that a shared intracellular Ca2+ pool is sensitive to the opioid, bradykinin and muscarinic receptor agonists; however, a specific phospholipase C might be responsible for each receptor activation.

摘要

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