title: Gastric secretion.
abstract: OBJECTIVE
  This review summarizes the past year's literature regarding the neural, paracrine, hormonal, and intracellular regulation of gastric acid secretion.
  
  
  RESULTS
  Gastric acid facilitates the digestion of protein as well as the absorption of iron, calcium, vitamin B12, and certain medications. High gastric acidity, in combination with pepsin and lipase, kills ingested microorganisms and may play a role in preventing bacterial overgrowth, enteric infection, and possibly spontaneous bacterial peritonitis, community-acquired pneumonia, and infection with Mycobacterium tuberculosis. Stimulants of acid secretion include histamine, gastrin, acetylcholine, and ghrelin. Inhibitors include somatostatin, gastric inhibitory polypeptide, calcitonin gene-related peptide, and adrenomedullin. Helicobacter pylori stimulates or inhibits depending upon the time course of infection and the area of the stomach predominantly infected. Proteins implicated in H-K-ATPase membrane trafficking include myosin IIB, F-actin, ezrin, and Rab GTPases.
  
  
  CONCLUSIONS
  Our understanding of the regulation of gastric acid secretion continues to advance. Such knowledge is crucial for the management of acid-peptic disorders and the development of novel medications, such as cholecystokinin-2 receptor antagonists.
authors.affiliation: aDivision of Gastroenterology, Department of Medicine, Virginia Commonwealth University Health System bDivision of Gastroenterology, Department of Medicine, Hunter Holmes McGuire Veterans Affairs Medical Center, Richmond, Virginia, USA.
authors.forename: Mitchell L
authors.initials: ML
authors.lastname: Schubert
mesh_terms: D000109:Acetylcholine / Q000378:metabolism; D001692:Biological Transport; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000378:metabolism* / Q000382:microbiology; D005755:Gastrins / Q000378:metabolism; D054439:Ghrelin / Q000378:metabolism; D017506:H(+)-K(+)-Exchanging ATPase / Q000378:metabolism*; D016481:Helicobacter Infections / Q000378:metabolism* / Q000382:microbiology / Q000503:physiopathology; D016480:Helicobacter pylori / Q000472:pathogenicity; D006632:Histamine / Q000378:metabolism; D006635:Histamine H2 Antagonists / Q000627:therapeutic use*; D006801:Humans; D010295:Parietal Cells, Gastric / Q000378:metabolism*; D013270:Stomach / Q000382:microbiology / Q000503:physiopathology
chemical_list: D005755:Gastrins; D054439:Ghrelin; D006635:Histamine H2 Antagonists; D006632:Histamine; D017506:H(+)-K(+)-Exchanging ATPase; D000109:Acetylcholine