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CFTR and its key role in in vivo resting and luminal acid-induced duodenal HCO3-secretion
Department of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Hannover, Germany.
Vise andre og tillknytning
2008 (engelsk)Inngår i: Acta Physiologica, ISSN 1748-1708, E-ISSN 1748-1716, Vol. 193, nr 4, s. 357-365Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Background and aims:  We investigated the role of the recently discovered, villous-expressed anion exchanger Slc26a6 (PAT1) and the predominantly crypt-expressed cystic fibrosis transmembrane regulator (CFTR) in basal and acid-stimulated murine duodenal HCO3 secretion in vivo, and the influence of blood HCO3 concentration on both.

Methods:  The proximal duodenum of anaesthetized mice was perfused in situ, and HCO3 secretion was determined by back-titration. Duodenal mucosal permeability was assessed by determining 51Cr-EDTA leakage from blood to lumen.

Results:  Compared with wild type (WT) littermates basal duodenal HCO3 secretory rates were slightly reduced in Slc26-deficient mice at low (∼21 mm), and markedly reduced at high blood HCO3 concentration (∼29 mm). In contrast, basal HCO3 secretion was markedly reduced in CFTR-deficient mice compared with WT littermates both at high and low blood HCO3 concentration. A short-term application of luminal acid increased duodenal HCO3 secretory rate in Slc26a6-deficient and WT mice to the same degree, but had no stimulatory effect in the absence of CFTR. Luminal acidification to pH 2.5 did not alter duodenal permeability.

Conclusions:  The involvement of Slc26a6 in basal HCO3 secretion in murine duodenum in vivo is critically dependent on the systemic acid/base status, and this transporter is not involved in acid-stimulated HCO3 secretion. The presence of CFTR is essential for basal and acid-induced HCO3 secretion irrespective of acid/base status. This suggests a coupled action of Slc26a6 with CFTR for murine basal duodenal HCO3 secretion, but not acid-stimulated secretion, in vivo.

sted, utgiver, år, opplag, sider
2008. Vol. 193, nr 4, s. 357-365
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URN: urn:nbn:se:uu:diva-16903DOI: 10.1111/j.1748-1716.2008.01854.xPubMedID: 18363901OAI: oai:DiVA.org:uu-16903DiVA, id: diva2:44674
Tilgjengelig fra: 2008-06-09 Laget: 2008-06-09 Sist oppdatert: 2018-01-12bibliografisk kontrollert

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