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MUCOSAL BIOLOGY

Independence of apical Cl^-/HCO₃^- exchange and anion conductance in duodenal HCO₃^- secretion

¹First Department of Medicine, Eberhard-Karls-Universität, 72076 Tübingen; and ²Zentrum Innere Medizin, Abteilung VI, Medizinische Hochschule Hannover, 30625 Hannover, Germany

Submitted 19 February 2003 ; accepted in final form 26 June 2003

Reduced gastrointestinal secretion contributes to malabsorption and obstructive syndromes in cystic fibrosis. The apical transport pathways in these organs have not been defined. We therefore assessed the involvement of apical Cl^-/ exchangers and anion conductances in basal and cAMP-stimulated duodenal secretion. Muscle-stripped rat and rabbit proximal duodena were mounted in Ussing chambers, and electrical parameters, secretion rates, and ³⁶Cl^-, ²²Na⁺, and ³H⁺ mannitol fluxes were assessed. mRNA expression levels were measured by a quantitative PCR technique. Removal of Cl^- from or addition of 1 mM DIDS to the luminal perfusate markedly decreased basal secretion but did not influence the secretory response to 8-bromo-cAMP, which was inhibited by luminal 5-nitro-2-(3-phenylpropylamino)-benzoate. Bidirectional ²²Na⁺ and ³⁶Cl^- flux measurements demonstrated an inhibition rather than a stimulation of apical anion exchange during cAMP-stimulated secretion. The ratio of Cl^- to in the anion secretory response was compatible with both Cl^- and being secreted via the CFTR anion channel. CFTR expression was very high in the duodenal mucosa of both species. We conclude that in rat and rabbit duodena, an apical Cl^-/ exchanger mediates a significant part of basal secretion but is not involved in the secretory response to cAMP analogs. The inhibitor profile, the strong predominance of Cl^- over in the anion secretory response, and the high duodenal CFTR expression levels suggest that a major portion of cAMP-stimulated duodenal secretion is directly mediated by CFTR.

cystic fibrosis transmembrane conductance regulator; 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid; 5-nitro-2-(3-phenylpropylamino)-benzoate; bicarbonate; cystic fibrosis; intestine

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