Functional interactions of HCO3- with cystic fibrosis transmembrane conductance regulator

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

Research output: Contribution to journalReview article

8 Citations (Scopus)


Disruption of normal cystic fibrosis transmembrane conductance regulator- (CFTR)-mediated Cl(-) transport is associated with cystic fibrosis (CF). CFTR is also required for HCO(3)(-) transport in many tissues such as the lungs, gastro-intestinal tract, and pancreas, although the exact role CFTR plays is uncertain. Given the importance of CFTR in HCO(3)(-) transport by so many CF-affected organ systems, it is perhaps surprising that relatively little is known about the interactions of HCO(3)(-) ions with CFTR. We have used patch clamp recordings from native pancreatic duct cells to study HCO(3)(-) permeation and interaction with CFTR. Ion selectivity studies shows that CFTR is between 3-5 times more selective for Cl(-) over HCO(3)(-). In addition, extracellular HCO(3)(-) has a novel inhibitory effect on cAMP-stimulated CFTR currents carried by Cl(-). The block by HCO(3)(-) was rapid, relatively independent of voltage and occurred over the physiological range of HCO(3)(-) concentrations. These data show that luminal HCO(3)(-) acts as a potent regulator of CFTR, and suggests that inhibition involves an external anion-binding site on the channel. This work has implications not only for elucidating mechanisms of HCO(3)(-) transport in epithelia, but also for approaches used to treat CF.

Original languageEnglish
Pages (from-to)207-11
Number of pages5
JournalJOP : Journal of the pancreas
Issue number4 Suppl
Publication statusPublished - Jul 2001


  • Animals
  • Bicarbonates/metabolism
  • Chlorides/metabolism
  • Cystic Fibrosis Transmembrane Conductance Regulator/physiology
  • Humans


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