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Volume 381, Issue 1-2 p. 47-52
Research letter
Free Access

Wild type but not ΔF508 CFTR inhibits Na+ conductance when coexpressed in Xenopus oocytes

M. Mall

M. Mall

Physiologisches Institut der Albert-Ludwigs-Universität Freiburg, Hermann-Herder-Str. 7, D79104 Freiburg, Germany

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A. Hipper

A. Hipper

Physiologisches Institut der Albert-Ludwigs-Universität Freiburg, Hermann-Herder-Str. 7, D79104 Freiburg, Germany

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R. Greger

Corresponding Author

R. Greger

Physiologisches Institut der Albert-Ludwigs-Universität Freiburg, Hermann-Herder-Str. 7, D79104 Freiburg, Germany

Corresponding author. Fax: (49) (761) 203-5191.Search for more papers by this author
K. Kunzelmann

K. Kunzelmann

Physiologisches Institut der Albert-Ludwigs-Universität Freiburg, Hermann-Herder-Str. 7, D79104 Freiburg, Germany

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First published: February 26, 1996
Citations: 111

Abstract

Airway epithelial cells bearing mutations of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) possess an increased Na+ conductance along with their well described defect of cAMP dependent Cl conductance. Currently it is not clear, how this occurs, and whether it is due to a CFTR control of epithelial Na+ conductances which might be defective in CF patients. In the present study, we have tried to identify possible interactions between both CFTR and the epithelial Na+ conductance by overexpressing respective cRNAs in Xenopus oocytes. The expression of all three (α, β, γ) subunits of the rat epithelial Na+ channel (rENaC) and wild type (wt) CFTR resulted in the expected amiloride sensitive Na+ and IBMX (1 mmol/l) activated Cl currents, respectively. The amiloride sensitive Na+ conductance was, however, inhibited when the wt-CFTR Cl conductance was activated by phosphodiesterase inhibition (IBMX). In contrast, IBMX had no such effect in ΔF508 and Na+ channels coexpressing oocytes. These results suggest that wt-CFTR, but not ΔF508-CFTR, is a cAMP dependent downregulator of epithelial Na+ channels. This may explain the higher Na+ conductance observed in airway epithelial cells of CF patients.