Basal and PGE2-stimulated duodenal bicarbonate secretion in the rat in vivo.

We studied basal and prostaglandin E2 (PGE2)-stimulated duodenal HCO3- transport in the rat in vivo both in the presence and absence of a concentration gradient for HCO3- from blood to lumen. Basal HCO3- transport was not reduced when the luminal solution was changed from one containing 0 mM HCO3- to one containing 22 mM HCO3- either at pH 9.0 or 7.5. Thus basal duodenal HCO3- transport in rats is independent of a blood-to-lumen HCO3- concentration gradient, which indicates an energy-dependent process with little passive flux of HCO3-. Luminal or intravenous administration of PGE2 significantly (P less than 0.01) increased HCO3- secretion into a HCO3(-)-free luminal solution but had no effect on HCO3- secretion into luminal solutions containing 22 mM HCO3-, either at pH 9.0 or 7.5. Therefore prostaglandins may act by increasing passive flux of HCO3- rather than by stimulating energy-dependent duodenal HCO3- transport.