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-MSH prevents impairment in renal function and dysregulation of AQPs and Na-K-ATPase in rats with bilateral ureteral obstruction

¹The Water and Salt Research Center, ²Institute of Clinical Medicine, and ³Institute of Anatomy, University of Aarhus, Aarhus; ⁴Department of Biochemistry and Cell Biology, School of Medicine, Kyungpook National University, Taegu, Korea; ⁵Department of Biological Psychiatry, Institute for Basic Psychiatric Research, Risskov; ⁶Department of Pharmacology, University of Copenhagen, Copenhagen; ⁷Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland; and ⁸Department of Clinical Physiology and Nuclear Medicine, Aarhus University Hospital-Skejby, Aarhus N, Denmark

Submitted 2 August 2004 ; accepted in final form 22 September 2005

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 aquaporins (AQPs) and Na-K-ATPase in the kidney in response to 24 h 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. Forty-eight hours after BUO-R demonstrated that -MSH treatment almost completely prevented the decrease in GFR (nontreated: 271 ± 50; -MSH: 706 ± 85; sham: 841 ± 105 µl·min^–1·100 g body wt^–1, P < 0.05) and ERPF (nontreated: 1,139 ± 217; -MSH: 2,598 ± 129; sham: 2,633 ± 457 µl·min^–1·100 g body wt^–1, P < 0.05). -MSH treatment also partly prevented the downregulation of AQP1 and Na-K-ATPase expression in rats after BUO-R for 48 h. 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.

urinary tract obstruction; water channels; sodium pump; urinary concentrating defect

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