Bicarbonate transport by rabbit duodenum in vitro: effect of vasoactive intestinal polypeptide, prostaglandin E2, and cyclic adenosine monophosphate.

Abstract

Duodenal surface cells secrete bicarbonate that provides a barrier against injury. The current experiments were performed to identify duodenal bicarbonate regulatory and transport pathways. Rabbit proximal duodenal mucosa were mounted in chambers under short-circuited conditions. Bicarbonate transport, short-circuit current (Isc), and potential difference (PD) were quantitated in response to prostaglandin E2 (PGE2), vasoactive intestinal polypeptide (VIP), and dibutyryl cyclic adenosine monophosphate (db-cAMP). Anoxia (N2), 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) and Cl(-)-free solutions, ouabain, and Na-free solutions were also studied, as was the effect of VIP and PGE2 on duodenocyte cAMP. PGE2, VIP, db-cAMP, and theophylline significantly increased bicarbonate secretion, Isc, and PD. Ouabain, Na(+)-free bathing solutions, and anoxia (N2) inhibited the responses. DIDS and Cl(-)-free solutions abolished the PGE2-induced response, reduced the response to VIP by about 50%, and had no effect on the response to db-cAMP. After PGE2 and VIP, cAMP concentration increased, yet was likely independent of bicarbonate secretion. Mammalian duodenal HCO3- transport requires Na+, Na+/K(+)-adenosine triphosphatase and O2-dependent metabolic pathways and is stimulated by PGE2, VIP, and cAMP, acting by distinct pathways.