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1 First Department of Medicine, Eberhard-Karls-Universitat, Tubingen, Germany
2 First Department of Medicine, Eberhard-Karls-Universitat, Tubingen, Germany; Zentrum Innere Medizin, Abteilung VI, Medizinische Hochschule Hannover, Hannover, Germany
* To whom correspondence should be addressed. E-mail: seidler.ursula{at}mh-hannover.de.
Reduced gastrointestinal HCO3- secretion contributes to malabsorption and obstructive syndromes in cystic fibrosis. The apical HCO3- transport pathways in these organs have not been defined. We therefore assessed the involvement of apical Cl-/HCO3- exchangers and anion con-ductances in basal and cAMP-stimulated duodenal HCO3- secretion. Muscle-stripped rat and rabbit proximal duodenum was mounted in Ussing-chambers and electrical parameters, HCO3- secretion rates, and 35Cl- and 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 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) to the luminal perfusate markedly decreased basal HCO3- secretion, but did not influence the HCO3- secretory response to 8-Br-cAMP, which was inhibited by luminal 5-nitro-2-(3-phenylpropylamino)-benzoate (NPPB). Bidi-rectional 22Na+ and 36Cl- flux measurements demonstrated an inhibition rather than a stimulation of apical anion exchange during cAMP-stimulated HCO3- secretion. The ratio of Cl-/HCO3- in the anion secretory response was compatible with both Cl- and HCO3- being secreted via the CFTR (cystic fibrosis transmembrane regulator) anion channel. CFTR expression was very high in the duodenal mucosa of both species. We conclude that in rat and rabbit duodenum, an apical Cl-/HCO3- exchanger mediates a significant part of basal HCO3- secretion, but is not involved in the HCO3- secretory response to cAMP-analogues. The inhibitor profile, the strong predominance of Cl- over HCO3- in the anion secretory response, and the high duodenal CFTR expres-sion levels suggest that a major portion of cAMP-stimulated duodenal HCO3- secretion is di-rectly mediated by CFTR.
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