Hogan D L, Yao B, Barrett K E, Isenberg J I
Department of Medicine, University of California, School of Medicine, San Diego, USA.
Gastroenterology. 1995 Jun;108(6):1676-82. doi: 10.1016/0016-5085(95)90128-0.
BACKGROUND/AIMS: The gastroduodenal epithelium is protected from acid peptic damage by an adherent mucus-bicarbonate layer. Bicarbonate is secreted by the surface epithelial cells into this mucus layer. Patients with duodenal ulcer disease have impaired proximal duodenal bicarbonate secretion. Mast cells, present in large numbers in the duodenal mucosa, release a number of inflammatory mediators, including histamine. Release of such mast cell mediators has been implicated in ulcer disease. In this study, the ability of histamine to regulate bicarbonate secretion was examined.
Bicarbonate secretion by rabbit proximal duodenal mucosa was examined in vitro, and the effects of histamine, its agonists, and its antagonists were studied.
Histamine essentially eliminated prostaglandin E2-stimulated duodenal mucosal bicarbonate secretion, an effect reversed both by the neurotoxin, tetrodotoxin, and the histamine H2-receptor antagonist, cimetidine, as well as reproduced by the H2-receptor agonist, dimaprit.
In addition to the stimulatory action of histamine on gastric acid secretion, histamine expresses an additional antidefensive action by inhibiting prostaglandin E2-stimulated duodenal epithelial bicarbonate secretion. This effect of histamine is likely mediated via H2 receptors located on enteric nerves.
