Regulation of gastric acid secretion

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Abstract

This review focuses on studies published in the past year that improve our understanding of the central, peripheral, and intracellular pathways and mechanisms that regulate gastric acid secretion. Gastrin, the main hormonal stimulant of acid secretion, is released during ingestion of a meal by the activation of vagal and intramural neurons, and it binds to gastrin/cholecystokinin- B (CCK-B) receptors on parietal cells, enterochromaffin- like (ECL) cells, somatostatin cells, and vagal afferent neurons. Gastrin is also responsible for maintenance of the oxyntic mucosa, particularly the proliferation of parietal and ECL cells. The trophic effects of gastrin are mediated through CCK-B and other receptors. Somatostatin is the primary inhibitor of acid secretion. Somatostatin cells exert a tonic paracrine restraint on parietal, ECL, and gastrin cells. Histamine, acting in a paracrine fashion, stimulates acid secretion directly by interacting with H2 receptors on parietal cells and indirectly by activating H3 receptors coupled to inhibition of somatostatin secretion. Parietal cell secretion is increased by activation of intracellular adenosine 3',5'-cyclic monophosphate- and calcium-dependent signaling systems that activate downstream protein kinases, ultimately leading to fusion and activation of H+K+-adenosinetriphosphatase, the proton pump

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