Abstract
Proximal duodenum isolated from the bullfrog actively transports HCO3−, into the lumen, a process which is inhibited by acetazolamide and indomethacin and stimulated by prostaglandins (Flemström 1979, 1980a). Duodenal mucosa in this animal is devoid of Brunner glands, indicating that active HCO3− transport is a property of the surface epithelial cells. HCO3− is secreted by duodenal epithelium also in the dog in vivo and acetazolamide decreases the rate of loss of intraduodenally instilled acid in this species (Harmon, Woods & Gurll 1978). These results suggest that epithelial HCO3− transport contributes to duodenal disposal of luminal acid. The ability of gastric inhibitory peptide (GIP) to inhibit gastric emptying and acid secretion (Pearce, Polak & Bloom 1977) should decrease delivery of H+ions into the duodenum. The latter may be indicative of an ulceroprotective function and made it of interest to examine the effects of GIP on duodenal epithelial HCO3− transport.
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