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Am J Physiol Renal Physiol 277: F413-F427, 1999;
0363-6127/99 $5.00
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Vol. 277, Issue 3, F413-F427, September 1999

Reduced abundance of aquaporins in rats with bilateral ischemia-induced acute renal failure: prevention by alpha -MSH

Tae-Hwan Kwon1, Jørgen Frøkiaer2, Patricia Fernández-Llama3, Mark A. Knepper3, and Søren Nielsen1

1 Department of Cell Biology, Institute of Anatomy, University of Aarhus; 2 Department of Clinical Physiology, Aarhus University Hospital and Institute of Experimental Clinical Research, DK-8000 Aarhus, Denmark; and 3 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892

We examined the effect of temporary renal ischemia (30 min or 60 min) and reperfusion (1 day or 5 days) on the expression of renal aquaporins (AQPs) and urinary concentration in rats with bilateral ischemia-induced acute renal failure (ARF). Next, we tested whether reducing ischemia/reperfusion (I/R) injury by treatment with alpha -melanocyte stimulating hormone (alpha -MSH) affects the expression of AQPs and urine output. Rats with ARF showed significant renal insufficiency, and urinary concentration was markedly impaired. In rats with mild ischemic injury (30 min), urine output increased significantly to a maximum at 48 h, and then nearly normalized within 5 days. Consistent with this, semiquantitative immunoblotting revealed that kidney AQP1 and AQP2 abundance was significantly decreased after 24 h to 30 ± 5% and 40 ± 11% (n = 8) of controls (n = 9), respectively (P < 0.05). Five days after ischemia, AQP2 abundance was not significantly decreased and urine output was normalized. In contrast, severe ischemic injury (60 min) resulted in a marked reduction in urine output at 24 h, despite a significant decrease in urine osmolality and solute-free water reabsorption, TcH2O. AQP1 and AQP2 abundance was markedly decreased to 51 ± 5% and 31 ± 9% (n = 10) of controls (n = 8) at 24 h (P < 0.05). After 5 days, the rats developed gradually severe polyuria and had very low AQP2 and AQP1 levels [11 ± 4% and 6 ± 2% (n = 5) of controls (n = 8), respectively; P < 0.05]. A similar reduction was observed for AQP3. The reduction in AQP expression in the proximal tubule and inner medullary collecting duct was confirmed by immunocytochemistry. Next, we found that intravenous alpha -MSH treatment of rats with ARF significantly reduced the ischemia-induced downregulation of renal AQPs and reduced the polyuria. In conclusion, the I/R injury is associated with markedly reduced expression of the collecting duct and proximal tubule AQPs, in association with an impairment of urinary concentration. Moreover, alpha -MSH treatment significantly prevented the reduction in expression of AQPs and renal functional defects. Thus decreased AQP expression is likely to contribute to the impairment in urinary concentration in the postischemic period.

acute tubular necrosis; alpha -melanocyte stimulating hormone; collecting duct; proximal tubule; urinary concentration mechanism


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