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Gastric secretion

Schubert, Mitchell L

Current Opinion in Gastroenterology: November 2007 - Volume 23 - Issue 6 - p 595–601
doi: 10.1097/MOG.0b013e3282f03462
Stomach and duodenum: Edited by Mitchell L. Schubert

Purpose of review This review summarizes the past year's literature regarding the regulation of gastric exocrine and endocrine secretion.

Recent findings Gastric acid secretion is tightly regulated by overlapping neural, hormonal, paracrine, and intracellular pathways in order to achieve the correct amount of acid secretion required by the specific situation. Too little acid can interfere with the absorption of iron, calcium, vitamin B12, and certain drugs as well as predispose to enteric infection, bacterial overgrowth, and gastric malignancy. Too much acid can induce esophageal, gastric, and duodenal injury. Gastrin, histamine, acetylcholine, and ghrelin stimulate whereas somatostatin, cholecystokinin, atrial natriuretic peptide, and nitric oxide inhibit acid secretion. Most patients infected with Helicobacter pylori manifest a pangastritis and produce less than normal amounts of acid; those with antral predominant gastritis, however, are hypergastrinemic and produce increased amounts of acid. Improved understanding of the channels and receptors that are required for and regulate H+K+-ATPase activity should lead to the development of novel antisecretory agents.

Summary A better understanding of the pathways regulating gastric secretions should lead to new strategies to prevent and treat a variety of gastric disorders such as gastroesophageal reflux disease, autoimmune gastritis, gastric cancer, and functional dyspepsia.

Department of Medicine, Division of Gastroenterology, Virginia Commonwealth University's Medical College of Virginia and McGuire Veterans Affairs Medical Center, Richmond, Virginia, USA

Correspondence to Mitchell L. Schubert, MD, McGuire VAMC; code 111N, Gastroenterology Division, 1201 Broad Rock Blvd., Richmond, VA 23249, USA Tel: +1 804 675 5021; fax: +1 804 675 5816; e-mail:

© 2007 Lippincott Williams & Wilkins, Inc.