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Non‐specific activation of the epithelial sodium channel by the CFTR chloride channel
Author(s) -
Nagel Georg,
Szellas Tanjef,
Riordan John R,
Friedrich Thomas,
Hartung Klaus
Publication year - 2001
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1093/embo-reports/kve045
Subject(s) - epithelial sodium channel , cystic fibrosis transmembrane conductance regulator , chloride channel , cystic fibrosis , chemistry , patch clamp , extracellular , stimulation , sodium , microbiology and biotechnology , mutant , biophysics , medicine , endocrinology , biochemistry , biology , gene , receptor , organic chemistry
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.