Effects of Slc26a6 deletion and CFTR inhibition on HCO3- secretion by mouse pancreatic duct

  • Song Ying
    Second Clinical College of Norman Bethune Medical Division, Jilin University Department of Human Nutrition, Nagoya University Graduate School of Medicine
  • Ishiguro Hiroshi
    Department of Human Nutrition, Nagoya University Graduate School of Medicine
  • Yamamoto Akiko
    Department of Human Nutrition, Nagoya University Graduate School of Medicine
  • Xiang Jin Chun
    Second Clinical College of Norman Bethune Medical Division, Jilin University
  • Kondo Takaharu
    Department of Human Nutrition, Nagoya University Graduate School of Medicine

Search this article

Abstract

Pancreatic duct epithelium secretes HCO3--rich fluid, which is dependent on cystic fibrosis transmembrane conductance regulator (CFTR). HCO3- transport across the apical membrane is thought to be mediated by both SLC26A6 Cl--HCO3- exchange and CFTR HCO3- conductance. In this study we examined the relative contribution and interaction of SLC26A6 and CFTR in apical HCO3- transport. Interlobular pancreatic ducts were isolated from slc26a6 null mice. Intracellular pH (pHi) was measured by BCECF microfluorometry. Duct cells were stimulated with forskolin and alkalinized by acetate pre-pulse in the presence of HCO3--CO2. Apical HCO3- secretion was estimated from the recovery rate of pHi from alkaline load. When the lumen was perfused with high-Cl- solution, the rate of apical HCO3- secretion was increased by luminal application of CFTRinh-172 in ducts from wild-type mice but it was decreased in ducts from slc26a6 -/- mice. This suggests that slc26a6 and CFTR compensate/compete with each other for apical HCO3- secretion with high Cl- in the lumen. With high HCO3- in the lumen, luminal CFTRinh-172 reduced the rate of apical HCO3- secretion in both wild-type and slc26a6 -/- ducts. This suggests that HCO3- conductance of CFTR mediates a significant portion of apical HCO3- secretion with high HCO3- in the lumen. J. Med. Invest. 56 Suppl.: 332-335, December, 2009

Journal

References(15)*help

See more

Related Projects

See more

Details 詳細情報について

Report a problem

Back to top