HCO3- secretion and surface pH gradient in rat duodenum exposed to luminal acid.
A pH gradient is maintained at the surface of rat duodenum exposed to luminal acid. The alkalinity and thickness of this gradient are dependent on the rate of surface epithelial HCO3- secretion (transport into the lumen). Acidification of the luminal solution stimulates HCO3- secretion and enhances the alkalinity at the mucosal surface by a mechanism dependent on endogenous prostaglandin synthesis. This stimulated HCO3- secretion is quantitatively sufficient to maintain neutrality at the epithelial surface of the mucosa even in the presence of as high luminal acidity as pH 2.0, which is the maximal 'physiologic' acidity within human duodenal bulb. Exogenous prostaglandin E2 increases HCO3- secretion as well as the dimensions of the pH gradient, which may, in part, account for its cytoprotective actions in gastroduodenal mucosa. The findings suggest that epithelial HCO3- secretion in the duodenal mucosa has a protective function by forming an unstirred alkaline layer at the mucosal surface which impedes the diffusion of luminal acid into the mucosa.
D000086:Acetazolamide / Q000494:pharmacology; D000818:Animals; D001241:Aspirin / Q000494:pharmacology; D001639:Bicarbonates / Q000378:metabolism*; D015232:Dinoprostone; D004386:Duodenum / Q000187:drug effects / Q000378:metabolism*; D005744:Gastric Acid / Q000378:metabolism*; D006863:Hydrogen-Ion Concentration; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism*; D011458:Prostaglandins E / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D001639:Bicarbonates; D011458:Prostaglandins E; D015232:Dinoprostone; D000086:Acetazolamide; D001241:Aspirin