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 HCO(3)(-) secretion in vivo, and the influence of blood HCO(3)(-) concentration on both. METHODS: The proximal duodenum of anaesthetized mice was perfused in situ, and HCO(3)(-) secretion was determined by back-titration. Duodenal mucosal permeability was assessed by determining (51)Cr-EDTA leakage from blood to lumen. RESULTS: Compared with wild type (WT) littermates basal duodenal HCO(3)(-) secretory rates were slightly reduced in Slc26-deficient mice at low ( approximately 21 mm), and markedly reduced at high blood HCO(3)(-) concentration ( approximately 29 mm). In contrast, basal HCO(3)(-) secretion was markedly reduced in CFTR-deficient mice compared with WT littermates both at high and low blood HCO(3)(-) concentration. A short-term application of luminal acid increased duodenal HCO(3)(-) 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 HCO(3)(-) secretion in murine duodenum in vivo is critically dependent on the systemic acid/base status, and this transporter is not involved in acid-stimulated HCO(3)(-) secretion. The presence of CFTR is essential for basal and acid-induced HCO(3)(-) secretion irrespective of acid/base status. This suggests a coupled action of Slc26a6 with CFTR for murine basal duodenal HCO(3)(-) secretion, but not acid-stimulated secretion, in vivo.
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 HCO(3)(-) secretion in vivo, and the influence of blood HCO(3)(-) concentration on both. METHODS: The proximal duodenum of anaesthetized mice was perfused in situ, and HCO(3)(-) secretion was determined by back-titration. Duodenal mucosal permeability was assessed by determining (51)Cr-EDTA leakage from blood to lumen. RESULTS: Compared with wild type (WT) littermates basal duodenal HCO(3)(-) secretory rates were slightly reduced in Slc26-deficientmice at low ( approximately 21 mm), and markedly reduced at high blood HCO(3)(-) concentration ( approximately 29 mm). In contrast, basal HCO(3)(-) secretion was markedly reduced in CFTR-deficient mice compared with WT littermates both at high and low blood HCO(3)(-) concentration. A short-term application of luminal acid increased duodenal HCO(3)(-) 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 HCO(3)(-) secretion in murine duodenum in vivo is critically dependent on the systemic acid/base status, and this transporter is not involved in acid-stimulated HCO(3)(-) secretion. The presence of CFTR is essential for basal and acid-induced HCO(3)(-) secretion irrespective of acid/base status. This suggests a coupled action of Slc26a6 with CFTR for murine basal duodenal HCO(3)(-) secretion, but not acid-stimulated secretion, in vivo.
Authors: Antonius L J J Bronckers; Don M Lyaruu; Jing Guo; Marcel J C Bijvelds; Theodore J M Bervoets; Behrouz Zandieh-Doulabi; Juan F Medina; Zhu Li; Yan Zhang; Pamela K DenBesten Journal: Eur J Oral Sci Date: 2014-12-30 Impact factor: 2.612
Authors: Julio C Chávez; Enrique O Hernández-González; Eva Wertheimer; Pablo E Visconti; Alberto Darszon; Claudia L Treviño Journal: Biol Reprod Date: 2012-01-19 Impact factor: 4.285