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pubmed-article:1404976pubmed:abstractTextTreatment of isolated parietal cells from guinea pig gastric mucosa with ethanol caused a rapid increase in [Ca2+]i and concomitant decrease in the capacity for carbachol-stimulated acid secretion in a dose dependent manner. Carbachol rapidly increased the [Ca2+]i from trimethoxybenzoic acid 8-(diethylamino)-octyl ester sensitive intracellular pool. In contrast, the increase with ethanol was through La3+ sensitive Ca2+ channel from external source, which suppressed the Ca2+ response subsequently stimulated with carbachol. Pretreatment of the cells with EGTA or La3+ completely prevented the elevation of [Ca2+]i with ethanol and preserved the Ca2+ response to carbachol. These findings indicate that ethanol-induced elevation of [Ca2+]i may desensitize the stimulation of carbachol. Furthermore, treatment of the parietal cells with ethanol increased the activity of protein kinase C in both cytosolic and membrane fractions of the cells. Activation of protein kinase C with phorbol diester suppressed the capacity for acid secretion. These results suggest that ethanol may inhibit the carbachol-stimulated acid secretion through the desensitization of Ca2+ response and the activation of protein kinase C.lld:pubmed
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pubmed-article:1404976pubmed:pagination1484-90lld:pubmed
pubmed-article:1404976pubmed:dateRevised2011-8-2lld:pubmed
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pubmed-article:1404976pubmed:articleTitle[Calcium-dependent signaling of acid secretion in isolated parietal cells from guinea pigs and its modification by ethanol].lld:pubmed
pubmed-article:1404976pubmed:affiliationDepartment of Preventive Medicine, Kyoto Prefectural University of Medicine.lld:pubmed
pubmed-article:1404976pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:1404976pubmed:publicationTypeEnglish Abstractlld:pubmed
pubmed-article:1404976pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed