Gastric secretion

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Abstract
Purpose of review The purpose of this chapter is to summarize and place into perspective the past year's literature regarding the regulation of gastric exocrine and endocrine secretion. Recent findings To prevent acid and pepsin from overwhelming mucosal defense mechanisms and causing injury, the secretion of gastric acid is precisely regulated by a variety of central (eg, neuropeptide Y, corticotropin-releasing factor, and neuromedin U) and peripheral (eg, gastrin, histamine, acetylcholine, somatostatin, cholecystokinin, calcitonin gene–related peptide, leptin, and parietal cell) pathways. These pathways regulate the acid-producing parietal cell directly and/or indirectly by regulating the secretion of histamine from enterochromaffin-like cells, gastrin from G cells, and somatostatin from D cells. Recently, genetically engineered mouse models have been used to reevaluate the neural, hormonal, and paracrine pathways that physiologically regulate acid secretion. Summary An improved understanding of the pathways and mechanisms regulating gastric acid secretion should lead to the development of novel therapies to prevent and treat acid-peptic disorders as well as circumvent the adverse effects of currently used antisecretory medications such as the acid rebound observed after discontinuation of proton pump inhibitors.

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