BACKGROUND: Duodenal surface cells secrete bicarbonate that provides a barrier against injury. The current experiments were performed to identify duodenal bicarbonate regulatory and transport pathways. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND: Duodenal surface cells secrete bicarbonate that provides a barrier against injury. The current experiments were performed to identify duodenal bicarbonate regulatory and transport pathways. METHODS: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. RESULTS: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. CONCLUSIONS: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.
Authors: Anne M Collaco; Robert L Jakab; Nadia E Hoekstra; Kisha A Mitchell; Amos Brooks; Nadia A Ameen Journal: Am J Physiol Gastrointest Liver Physiol Date: 2013-06-06 Impact factor: 4.052
Authors: U Seidler; I Blumenstein; A Kretz; D Viellard-Baron; H Rossmann; W H Colledge; M Evans; R Ratcliff; M Gregor Journal: J Physiol Date: 1997-12-01 Impact factor: 5.182
Authors: Bi-Guang Tuo; Zachary M Sellers; Anders J Smith; Kim E Barrett; Jon I Isenberg; Hui Dong Journal: Dig Dis Sci Date: 2004 Nov-Dec Impact factor: 3.199