Mar 27, 2001

Non-specific activation of the epithelial sodium channel by the CFTR chloride channel

EMBO Reports
G NagelK Hartung

Abstract

The genetic disease cystic fibrosis is caused by mutation of the gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR). Controversial studies reported regulation of the epithelial sodium channel (ENaC) by CFTR. We found that uptake of (22)Na(+) through ENaC is modulated by activation of CFTR in oocytes, coexpressing CFTR and ENaC, depending on extracellular chloride concentration. Furthermore we found that the effect of CFTR activation could be mimicked by other chloride channels. Voltage- and patch-clamp measurements, however, showed neither stimulation nor inhibition of ENaC-mediated conductance by activated CFTR. We conclude that the observed modulation of (22)Na(+) uptake by activated CFTR is due to the effect of CFTR-mediated chloride conductance on the membrane potential. These findings argue against the notion of a specific influence of CFTR on ENaC and emphasize the chloride channel function of CFTR.

Mentioned in this Paper

Epithelial sodium channel
Extracellular
CFTR protein, human
Proteins, Recombinant DNA
Uptake
PDZK1 gene
Cystic Fibrosis
Etiology
Mesothelium
Clamping Activity

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