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Articles in PresS, published online ahead of print September 11, 2002
Am J Physiol Gastrointest Liver Physiol, 10.1152/ajpgi.00283.2002
Submitted on July 15, 2002
Accepted on September 4, 2002
1 Department of Physiology, The University of Michigan, Ann Arbor, MI, USA
* To whom correspondence should be addressed. E-mail: lcsam{at}umich.edu.
Gastrin-deficient mice have impaired basal and agonist-stimulated gastric acid secretion. To analyze whether an intrinsic parietal cell defect contributed to the reduced acid secretion, we analyzed parietal cell calcium responses and acid secretory function in vitro. Parietal cells were purified by light scatter cell sorting, and calcium responses to gastrin, histamine, and carbachol were measured in gastrin-deficient and wild type preparations. Surprisingly, basal and histamine-induced calcium concentrations were higher in the mutant. [14C]aminopyrine uptake analysis in acutely isolated gastric glands revealed that basal acid accumulation was enhanced in gastrin-deficient preparations as well as upon treatment with carbachol or histamine. These results suggested that an intrinsic parietal cell defect was not responsible for the reduced acid secretion in gastrin-deficient mice. Flow cytometric analysis of dispersed, H+/K+-ATPase-immunostained gastric mucosal preparations revealed a marked increase in parietal cell number in gastrin-deficient mice, which may have accounted for the enhanced in vitro acid secretion detected in this study. Parietal cells were found to be significantly smaller in the mutant, suggesting that gastrin stimulation modulates parietal cell morphology.
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