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Gastric HCO3(-) transport (basal) studied in isolated amphibian mucosa and mammalian stomach in vivo amounts to 2-10% of maximal H+ secretion. Duodenal mucosa, devoid of Brunner's glands, transports HCO3(-) at a greater rate (per unit surface area) than either stomach or jejunum in vitro and in vivo. Gastric (but not duodenal) HCO3(-) transport is stimulated by dibutyryl cGMP, carbachol, and cholecystokinin and duodenal (but not gastric) transport by dibutyryl cAMP and gastric inhibitory peptide. Glucagon and E- and F-type prostaglandins stimulate, whereas histamine, gastrin, and secretin are without effect in both stomach and duodenum. Gastric transport very probably occurs by Cl--HCO3(-) exchange at the luminal membranes of the surface epithelial cells. In addition to this mechanism, the duodenum also transports HCO3(-) electrogenically. Lowering the luminal pH increases transport in both the stomach and duodenum. This response, probably mediated via both local production of prostaglandins and tissue-specific humoral agents, may be important in mucosal protection against acid. Metabolism-dependent transport of HCO3(-), stimulated by acid, seems quantitatively sufficient to account for all of the duodenal and most of the gastric mucosa's ability to remove luminal acid.

Gastroduodenal HCO3(-) transport: characteristics and proposed role in acidity regulation and mucosal protection