Carbamoylcholine and gastrin induce inositol lipid turnover in canine gastric parietal cells.
Carbamoylcholine and gastrin induce inositol lipid turnover in canine gastric parietal cells.
复制标题
氨基甲酰胆碱和胃泌素诱导犬胃壁细胞中的肌醇脂质周转。
DOI:
10.1152/ajpgi.1988.255.1.g99
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发表时间:
1988
期刊:
影响因子:
--
通讯作者:
Yamada,T
中科院分区:
文献类型:
--
作者:
Chiba,T;Fisher,SK;Park,J;Seguin,EB;Agranoff,BW;Yamada,T
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.