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Am J Physiol Renal Physiol (September 27, 2005). doi:10.1152/ajprenal.00084.2005
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Submitted on March 2, 2005
Accepted on September 25, 2005

Increased apical targeting of renal ENaC subunits and decreased expression of 11{beta}HSD2 in HgCl2-induced nephrotic syndrome in rats

Soo Wan Kim1, Sophie de Seigneux2, Martin C. Sassen2, JongUn Lee3, Jin Kim4, Mark A. Knepper5, Jorgen Frokiaer6, and Soren Nielsen2*

1 The Water and Salt Research Center, University of Aarhus, Aarhus C, Denmark; Research Institute of Medical Sciences, Chonnam National University Medical School, Gwangju, Korea, Republic of
2 The Water and Salt Research Center, University of Aarhus, Aarhus C, Denmark; Institute of Anatomy, University of Aarhus, Aarhus C, Denmark
3 Research Institute of Medical Sciences, Chonnam National University Medical School, Gwangju, Korea, Republic of
4 Department of Anatomy, The Catholic University of Korea, Seoul, Korea, Republic of
5 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland, USA
6 The Water and Salt Research Center, University of Aarhus, Aarhus C, Denmark; Institute of Clinical Medicine, Aarhus University Hospital, Aarhus N, Denmark

* To whom correspondence should be addressed. E-mail: sn{at}ana.au.dk.

Nephrotic syndrome is often accompanied by sodium retention and generalized edema. We hypothesize that dysregulation of epithelial sodium channel (ENaC) and/or of sodium (co)transporters may be responsible for the increased sodium retention associated with HgCl2 induced nephropathy. In addition we examined the hypothesis that the expression of type 2 11{beta}-hydroxysteroid dehydrogenase (11{beta}HSD2) is reduced contributing to the enhanced mineralocorticoid activity. Membranous nephropathy was induced in Brown Norway rats by repeated injections of HgCl2 (1 mg/kg, s.c.), while the control group received only vehicle. After 13 days of treatment, the abundance of ENaC subunits, sodium (co)transporters and 11{beta}HSD2 in kidney was examined by immunoblotting and immunohistochemistry. HgCl2 treatment induced marked proteinuria, hypoalbuminemia, decreased urinary sodium excretion and ascites. The protein abundance of {alpha}ENaC was increased in the cortex/outer stripe of outer medulla (OSOM) and inner stripe of the outer medulla (ISOM). The protein abundances of {beta}ENaC and {gamma}ENaC were decreased in the cortex/OSOM, while increased in the ISOM. Immunoperoxidase microscopy demonstrated increased targeting of ENaC subunits to the apical plasma membrane in the distal convoluted tubule (DCT2), connecting tubule, and cortical and medullary collecting duct segments. Moreover, 11{beta}HSD2 abundance was decreased in cortex/OSOM and ISOM. The protein abundances of NHE3, NKCC2 and NCC were decreased. Moreover, the abundance of the {alpha}-1 subunit of the Na,K-ATPase was decreased in the cortex/OSOM and ISOM, but remained unchanged in the inner medulla. These results suggest that increased apical targeting of ENaC subunits combined with diminished abundance of 11{beta}HSD2 may contribute to sodium retention associated with HgCl2-induced nephrotic syndrome. The decreased abundance of NHE3, NKCC2, NCC and Na,K-ATPase may play a compensatory role to promote sodium excretion.




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