The anion transporter Slc26a6 (Putative Anion Transporter-1) regulates CO2/HCO3- induced murine small intestinal fluid absorption

Physiology 2012 (Edinburgh) (2012) Proc Physiol Soc 27, PC96

Poster Communications: The anion transporter Slc26a6 (Putative Anion Transporter-1) regulates CO2/HCO3- induced murine small intestinal fluid absorption

W. Xia1,2, Y. Qin1,3, A. Singh1, R. Brigitte1, R. Engelhardt1, P. Song2, D. Tian3, M. Soleimani4, U. Seidler1

1. Dept. of Gastroenterology, Hannover Medical School, Hannover, Germany. 2. Key Lab of Combined Multiorgan Transplantation, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China. 3. 3Dept. of Gastroenterology, Tongji Hospital, Huazhong University of Science & Technology, Wuhan, China. 4. Center on Genetics of Transport and Epithelial Biology, University of Cincinnati, Cincinnati, Ohio, United States.

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Background: Slc26a6 (PAT-1), a multi anion transporter, is strongly expressed in the apical membrane of the upper small intestine. Data on its function are equivocal. Aim: To investigate if, under which conditions, and by what mechanisms, Slc26a6 contributes to intestinal fluid absorption in vivo. Methods: Small intestinal fluid absorption was assessed by single pass perfusion of 3 cm long, vascularly perfused jejunal segments in 2%-isoflurane anesthe-tized acid/base status controlled mice with prewarmed, isotonic solutions of different ionic compositions but constant pH of 7.4. The volume and pH of the inflowing and outflowing solution was measured. Results: WT jejunum absorbed fluid and acidified the lumen. Slc26a3 (DRA)-deficient jejunum absorbed less fluid than WT, and acidified the lumen more strongly, consistent with its action as a Cl-/HCO3- ex-changer. Slc26a6 (PAT-1)-deficient jejunum also absorbed less fluid, but resulted in less luminal acidification. Switching the luminal solution to a 5% CO2/HCO3- buffer strongly augmented fluid absorption in a PAT-1- and NHE3- but not DRA-dependent manner. Removal of luminal Na+ abolished fluid absorption in luminal NaCl but not in CO2/HCO3-, where the absorption became completely dependent on PAT-1 expression. In the absence of luminal Cl-, lu-minal CO2/HCO3- also augumented fluid absorption, but in this case, the increase in absorption was dependent on both PAT-1 and NHE3 expression, and was markedly increased in DRA-deficient jejunum. Conclusions: The results suggest that Slc26a6 (PAT-11) strongly augments CO2/HCO3-induced jejunal fluid absorption, likely operating in a 2 HCO3-/1 Cl- as well as 2 HCO3-/1 HCO3- mode.



Where applicable, experiments conform with Society ethical requirements.

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