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

Luminal acid (10 mM HCl) is a stimulant of surface epithelial HCO-3 transport in mammalian stomach and duodenum in vivo. To determine whether a humoral mechanism is involved in mediation of this response, amphibian 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 HCO-3 transport by one mucosa titrated (at pH 7.40) during exposure of the parallel tissue to luminal acid. In studies of fundic HCO-3 transport, H+ secretion was inhibited with the histamine H2-antagonist tiotidine (10(-4) M). Fundic luminal acid stimulated HCO-3 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 HCO-3 transport by both parallel duodenum (21 +/- 5%) and fundus (109 +/- 32%). Stimulation of HCO-3 transport occurred at higher luminal pH in duodenum (approximately 4.0) than in fundus (approximately 2.0). Thus, exposure to luminal acid releases humoral factor(s) capable of stimulating surface epithelial HCO-3 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.