Regulation of gastroduodenal HCO-3 transport by luminal acid in the frog in vitro

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Abstract
Luminal acid (10 mM HCl) is a stimulant of surface epithelial HCO3- transport in mammalian stomach and duodenum in vivo. To determine whether a humoral mechanism is involved in mediation of this response, amphibian [Rana catesbiana, Rana temporaria] fundic, antral or proximal duodenal mucosae were mounted in parallel in an in vitro chamber with their nutrient (serosal) surfaces facing a common solution. The mucosal surfaces were bathed by separate solutions and the rate of HCO3- transport by 1 mucosa titrated (at pH 7.40) during exposure of the parallel tissue to luminal acid was examined. In studies of fundic HCO3- transport, H+ secretion was inhibited with the histamine H2-antagonist tiotidine (10-4 M). Fundic luminal acid stimulated HCO3- transport by a parallel fundus (27 .+-. 6%) or antrum (53 .+-. 27%) but had no effect on a parallel duodenum. Antral luminal acid had no effect on a parallel antrum, indicating that the gastric stimulant is of fundic origin. Duodenal luminal acid increased HCO3- transport by both parallel duodenum (21 .+-. 5%) and fundus (109 .+-. 32%). Stimulation of HCO3- transport occurred at higher luminal pH in duodenum (.apprx. 4.0) than in fundus (.apprx. 2.0). Thus, exposure to luminal acid releases humoral factor(s) capable of stimulating surface epithelial HCO3- transport by both stomach and duodenum. The actions of these putative stimulants are in part tissue specific and they may be important in mediation of mucosal protection against luminal acid.