Activation of the epithelial Na+ channel (ENaC) requires CFTR Cl- channel function

M. M. Reddy, M. J. Light and P. M. Quinton ()
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M. M. Reddy: University of California, San Diego, School of Medicine
M. J. Light: University of California, San Diego, School of Medicine
P. M. Quinton: University of California, San Diego, School of Medicine

Nature, 1999, vol. 402, issue 6759, 301-304

Abstract: Abstract It is increasingly being recognized that cells coordinate the activity of separate ion channels that allow electrolytes into the cell. However, a perplexing problem in channel regulation has arisen in the fatal genetic disease cystic fibrosis, which results from the loss of a specific Cl- channel (the CFTR channel) in epithelial cell membranes1. Although this defect clearly inhibits the absorption of Na+ in sweat glands2,3, it is widely accepted that Na+ absorption is abnormally elevated in defective airways in cystic fibrosis4,5. The only frequently cited explanation for this hypertransport is that the activity of an epithelial Na+ channel (ENaC) is inversely related to the activity of the CFTR Cl- channel5,6,7. However, we report here that, in freshly isolated normal sweat ducts, ENaC activity is dependent on, and increases with, CFTR activity. Surprisingly, we also find that the primary defect in Cl- permeability in cystic fibrosis8 is accompanied secondarily by a Na+ conductance in this tissue that cannot be activated. Thus, reduced salt absorption in cystic fibrosis is due not only to poor Cl- conductance but also to poor Na+ conductance.

Date: 1999
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DOI: 10.1038/46297

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