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1 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Institute of Clinical Medicine, University of Aarhus, Aarhus, Denmark
2 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Institute of Anatomy, University of Aarhus, Aarhus, Denmark
3 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Taegu, Korea, Republic of
4 Department of Biological Psychiatry, Institute for Basic Psychiatric Research, Risskov, Denmark
5 Department of Pharmacology, University of Copenhagen, Copenhagen, Denmark
6 Institute of Clinical Medicine, University of Aarhus, Aarhus, Denmark
7 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, USA
8 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Institute of Clinical Medicine, University of Aarhus, Aarhus, Denmark; Department of Clinical Physiology and Nuclear Medicine, Aarhus University Hospital-Skejby, Aarhus, Denmark
* To whom correspondence should be addressed. E-mail: JF{at}KI.AU.DK.
The purpose of this study was to evaluate the effects of the anti-inflammatory hormone 
-
melanocyte stimulating hormone (-MSH) treatment on renal function and expression of AQPs and
Na,K-ATPase in the kidney in response to 24 hours of bilateral ureteral obstruction (BUO) or release of
BUO (BUO-R). In rats with 24 h BUO, immunoblotting revealed that downregulation of AQP2 and
AQP3 was attenuated (AQP2: 38 ± 5% vs. 13 ± 4%; AQP3: 44 ± 3% vs. 19 ± 4% of sham levels;
P<0.05), whereas downregulation of Na,K-ATPase was prevented by -MSH treatment (Na,K-ATPase:
94 ± 7% vs. 35 ± 5% of sham levels; P<0.05). Immunocytochemistry confirmed the changes in AQP1
and Na,K-ATPase expression. Renal tubular cell apoptosis was confirmed in BUO kidneys and -MSH
treatment virtually completely abolished apoptosis. Furthermore, we measured glomerular filtration rate
(GFR) and effective renal plasma flow (ERPF), respectively. 48 h after BUO-R demonstrated that -
MSH treatment almost completely prevented the decrease in GFR (non-treated: 271 ± 50
µl/min/100gbw; -MSH: 706 ± 85 µl/min/100gbw; sham: 841 ± 105 µl/min/100gbw, P<0.05) and ERPF
(non-treated: 1139 ± 217 µl/min/100gbw; -MSH: 2598 ± 129 µl/min/100gbw; sham: 2633 ± 457
µl/min/100gbw, P<0.05) 48 hours after release of BUO. -MSH treatment also partly prevented the
downregulation of AQP1 and Na,K-ATPase expression in rats after release of BUO for 48 hours. In
conclusion, -MSH treatment significantly prevents impairment in renal function, and also prevents
downregulation of AQP2, AQP3 and Na,K-ATPase during BUO or AQP1 and Na,K-ATPase after BUO-R,
demonstrating a marked renoprotective effect of -MSH treatment in conditions with urinary tract
obstruction.
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