The purpose of this review is to summarize the pertinent literature published in the past year regarding the regulation of gastric exocrine and endocrine secretion.
Gastric acid aids protein digestion; facilitates the absorption of iron, calcium, and vitamin B12; thwarts enteric infection; and prevents bacterial overgrowth. When levels of acid and proteolytic enzymes overwhelm the mucosal defense mechanisms, ulcers occur. To avoid damage under these harsh conditions, gastric acid must be finely regulated by overlapping neural (e.g. orexin, pituitary adenylate cyclase-activating polypeptide, nitric oxide, and galanin), hormonal (e.g. gastrin, cholecystokinin, and ghrelin), paracrine (e.g. histamine and somatostatin), and autocrine (e.g. transforming growth factor-α) pathways. The precise mechanisms whereby Helicobacter pylori induces perturbations in acid secretion are not known, but they seem to involve changes in somatostatin and perhaps ghrelin secretion. Acid secretion by parietal cells involves intracellular elevation of calcium and/or cyclic AMP, followed by a cascade that triggers translocation of the proton pump, H+K+-adenosine triphosphatase, from cytoplasmic tubulovesicles to the secretory canaliculi.
An improved understanding of the pathways and mechanisms regulating gastric acid secretion may lead to the development of new strategies to prevent and treat acid peptic disorders as well as circumvent the adverse effects of currently prescribed antisecretory medications.
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, McGuire VAMC; code 111N, Gastroenterology Division, 1201 Broad Rock Boulevard, Richmond, VA 23249, USA
Tel: 804 675 5021; fax: 804 675 5816; e-mail: Mitchell.Schubert@med.va.gov