Carbamoylcholine and gastrin induce inositol lipid turnover in canine gastric parietal cells

Am J Physiol. 1988 Jul;255(1 Pt 1):G99-105. doi: 10.1152/ajpgi.1988.255.1.G99.


The potential role of inositol phospholipid turnover in mediating acid secretion was examined in a preparation enriched for isolated canine gastric parietal cells. The stimulatory effects of carbamoylcholine (carbachol) and gastrin on parietal cell uptake of [14C]aminopyrine were linked to dose- and time-dependent selective reduction in cellular phosphatidylinositol content, although the specific fatty acid composition of the phosphoinositides was not altered. Analysis of [3H]inositol phosphates accumulated in cells prelabeled with [3H]inositol revealed an increase in labeled inositol trisphosphate by 5 min of incubation with either carbachol or gastrin. Furthermore, after preincubation of parietal cells in medium containing [32P]orthophosphate, the two secretagogues elicited a time-dependent decrease in 32P labeling of phosphatidylinositol 4,5-bisphosphate and concomitant increase in labeling of phosphatidic acid. These data demonstrate that the acid secretagogue actions of carbachol and gastrin are correlated with turnover of cellular inositol phospholipids in a preparation consisting predominantly of parietal cells.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aminopyrine / metabolism
  • Animals
  • Carbachol / pharmacology*
  • Dogs
  • Gastrins / pharmacology*
  • Histamine / pharmacology
  • Parietal Cells, Gastric / drug effects
  • Parietal Cells, Gastric / metabolism*
  • Phosphatidylinositols / metabolism*
  • Time Factors


  • Gastrins
  • Phosphatidylinositols
  • Aminopyrine
  • Histamine
  • Carbachol