Anion interactions with CFTR and consequences for HCO3- transport in secretory epithelia

M Gray, C O'Reilly, J Winpenny, B Argent

Research output: Contribution to journalReview article

4 Citations (Scopus)


We have been studying CFTR channels in guinea pig pancreatic duct cells and rather surprisingly found that luminal HCO3- had a pronounced inhibitory effect on cAMP-activated CFTR chloride currents. The block produced by HCO3- was rapid, voltage-independent and occurred over a physiological range of extracellular HCO3- concentrations. I- and ClO4- were also found to inhibit CFTR currents, but both were less effective than HCO3-. Although we have not identified how HCO3- is able to block CFTR our data suggests that an external anion-binding site on the channel itself is involved. Overall, our results show that luminal HCO3- acts as a potent inhibitor of CFTR channels (and by inference CFTR-mediated secretion), under normal physiological conditions. These data have implications not only for current models of pancreatic duct cell HCO3- transport, but also for other bicarbonate-secreting tissues, such as the liver, GI tract and lungs.

Original languageEnglish
Pages (from-to)S12-5
JournalJournal of the Korean Physical Society
Volume15 Suppl
Publication statusPublished - Aug 2000


  • Animals
  • Anions/metabolism
  • Bicarbonates/metabolism
  • Cystic Fibrosis Transmembrane Conductance Regulator/metabolism
  • Epithelial Cells/metabolism
  • Pancreatic Ducts/cytology


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