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Am J Physiol Gastrointest Liver Physiol 255: G99-G105, 1988;
0193-1857/88 $5.00
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AJP - Gastrointestinal and Liver Physiology, Vol 255, Issue 1 99-105, Copyright © 1988 by American Physiological Society

ARTICLES

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

T. Chiba, S. K. Fisher, J. Park, E. B. Seguin, B. W. Agranoff and T. Yamada
Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109-0362.

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.


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