In experimental nephrotic syndrome, urinary sodium excretion is decreased during the early phase of the disease. The molecular mechanism(s) leading to salt retention has not been completely elucidated. The rate-limiting constituent of collecting duct sodium transport is the epithelial sodium channel (ENaC). We examined the abundance of ENaC subunit mRNAs and proteins in puromycin aminonucleoside (PAN)-induced nephrotic syndrome. The time courses of urinary sodium excretion, plasma aldosterone concentration and proteinuria were studied in male Sprague–Dawley rats treated with a single dose of either PAN or vehicle. The relative amounts of αENaC, βENaC and γENaC mRNAs were determined in kidneys from these rats by real-time quantitative TaqMan PCR, and the amounts of proteins by Western blot. The kinetics of urinary sodium excretion and the appearance of proteinuria were comparable with those reported previously. Sodium retention occurred on days 2, 3 and 6 after PAN injection. A significant up-regulation of αENaC and βENaC mRNA abundance on days 1 and 2 preceded sodium retention on days 2 and 3. Conversely, down-regulation of αENaC, βENaC and γENaC mRNA expression on day 3 occurred in the presence of high aldosterone concentrations, and was followed by a return of sodium excretion to control values. The amounts of αENaC, βENaC and γENaC proteins were not increased during PAN-induced sodium retention. In conclusion, ENaC mRNA expression, especially αENaC, is increased in the very early phase of the experimental model of PAN-induced nephrotic syndrome in rats, but appears to escape from the regulation by aldosterone after day 3.
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March 13 2003
Epithelial sodium channel (ENaC) subunit mRNA and protein expression in rats with puromycin aminonucleoside-induced nephrotic syndrome
A. AUDIGÉ;
A. AUDIGÉ
1Division of Nephrology and Hypertension, Inselspital, University of Berne, Freiburgstrasse 3, 3010 Berne, Switzerland
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Z.R. YU;
Z.R. YU
1Division of Nephrology and Hypertension, Inselspital, University of Berne, Freiburgstrasse 3, 3010 Berne, Switzerland
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B.M. FREY;
B.M. FREY
1Division of Nephrology and Hypertension, Inselspital, University of Berne, Freiburgstrasse 3, 3010 Berne, Switzerland
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D.E. UEHLINGER;
D.E. UEHLINGER
1Division of Nephrology and Hypertension, Inselspital, University of Berne, Freiburgstrasse 3, 3010 Berne, Switzerland
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F.J. FREY;
F.J. FREY
1Division of Nephrology and Hypertension, Inselspital, University of Berne, Freiburgstrasse 3, 3010 Berne, Switzerland
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B. VOGT
1Division of Nephrology and Hypertension, Inselspital, University of Berne, Freiburgstrasse 3, 3010 Berne, Switzerland
Correspondence: Dr Bruno Vogt (e-mail [email protected]).
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Publisher: Portland Press Ltd
Received:
August 19 2002
Revision Received:
December 20 2002
Accepted:
January 24 2003
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society and the Medical Research Society © 2003
2003
Clin Sci (Lond) (2003) 104 (4): 389–395.
Article history
Received:
August 19 2002
Revision Received:
December 20 2002
Accepted:
January 24 2003
Citation
A. AUDIGÉ, Z.R. YU, B.M. FREY, D.E. UEHLINGER, F.J. FREY, B. VOGT; Epithelial sodium channel (ENaC) subunit mRNA and protein expression in rats with puromycin aminonucleoside-induced nephrotic syndrome. Clin Sci (Lond) 1 April 2003; 104 (4): 389–395. doi: https://doi.org/10.1042/cs1040389
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