Carbachol but not bradykinin blocks the enkephalin-induced calcium transient in human neuroblastoma SK-N-SH cells.
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.
Liu
T Y
TY
Department of Biochemistry, National Defense Medical Center, Taipei, Taiwan, ROC.
Chueh
S H
SH
D001920:Bradykinin / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology*; D002478:Cells, Cultured / Q000187:drug effects; D004745:Enkephalins / Q000494:pharmacology*; D006801:Humans; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D009447:Neuroblastoma / Q000188:drug therapy*
D004745:Enkephalins; D015544:Inositol 1,4,5-Trisphosphate; D002217:Carbachol; D001920:Bradykinin; D002118:Calcium