| Literature DB >> 6097421 |
Abstract
Duodenum is exposed to potential damage from acidopeptic secretions emptied from the stomach. In several mammalian species the duodenal mucosa was shown some 50 years ago to be better able to resist acid gastric juice than mucosa in more distal small intestine. Recent studies have identified HCO3- secretion originating from the surface epithelium, together with the ability of this epithelium to respond to intraluminal acid with a rise in HCO3- secretion, as important components of duodenal mucosal protection. Whether duodenal (Brunner's) glands also secrete some HCO3- is at present unknown. Secretion of HCO3- is stimulated up to 10-fold by the presence of luminal acid and is quantitatively sufficient to maintain neutrality at the mucosal cell surface at the lowest pH values encountered in the duodenum (approximately pH 2.0). Stimulation is mediated by mucosal production of prostaglandins, humoral factors and possibly neural mechanisms. The mucus gel adherent to the mucosa provides a physical basis for the standing pH gradient generated by epithelial HCO3- secretion. In vivo, mucosal blood flow supplies HCO3- to the epithelial cells and is particularly important at high (stimulated) rates of secretion.Entities:
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Year: 1984 PMID: 6097421 DOI: 10.1002/9780470720905.ch7
Source DB: PubMed Journal: Ciba Found Symp ISSN: 0300-5208