The cystic fibrosis transmembrane conductance regulator (CFTR) inhibits ENaC through an increase in the intracellular Cl- concentration

EMBO Rep. 2001 Nov;2(11):1047-51. doi: 10.1093/embo-reports/kve232. Epub 2001 Oct 17.

Abstract

Activation of the CFTR Cl- channel inhibits epithelial Na+ channels (ENaC), according to studies on epithelial cells and overexpressing recombinant cells. Here we demonstrate that ENaC is inhibited during stimulation of the cystic fibrosis transmembrance conductance regulator (CFTR) in Xenopus oocytes, independent of the experimental set-up and the magnitude of the whole-cell current. Inhibition of ENaC is augmented at higher CFTR Cl- currents. Similar to CFTR, ClC-0 Cl- currents also inhibit ENaC, as well as high extracellular Na+ and Cl- in partially permeabilized oocytes. Thus, inhibition of ENaC is not specific to CFTR and seems to be mediated by Cl-.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Chlorine / metabolism*
  • Chlorine / pharmacology
  • Cystic Fibrosis Transmembrane Conductance Regulator / metabolism*
  • Cystic Fibrosis Transmembrane Conductance Regulator / physiology*
  • Electrophysiology
  • Epithelial Cells / metabolism
  • Epithelial Sodium Channels
  • Oocytes / metabolism
  • RNA, Complementary / metabolism
  • Rats
  • Sodium / pharmacology
  • Sodium Channel Blockers*
  • Sodium Channels / metabolism*
  • Xenopus

Substances

  • Epithelial Sodium Channels
  • RNA, Complementary
  • Sodium Channel Blockers
  • Sodium Channels
  • Cystic Fibrosis Transmembrane Conductance Regulator
  • Chlorine
  • Sodium