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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 Department of Physiology and Pharmacology, University of Southern Denmark, Aarhus, Denmark
3 The Water and Salt Research Center, University of Aarhus, Aarhus, Denmark; Institute of Anatomy, University of Aarhus, Aarhus, Denmark
4 Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA
5 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.
Bilateral ureteral obstruction (BUO) is associated with marked changes in the expression of renal aquaporins (AQPs) and sodium transport proteins. To examine the role of prostaglandin in this response, we investigated whether 24 h BUO changed the expression of cyclooxygenases (COX-1 and -2) in the kidney and tested the effect of the selective COX-2 inhibitor parecoxib (5 mg/kg/day via osmotic minipumps) on AQPs and sodium transport. Sham and BUO kidneys were analyzed by semiquantitative immunoblotting and a subset of kidneys were perfusion fixed for immunocytochemistry. BUO caused a significant 14-fold induction of inner medullary COX-2 (14.40±1.8 vs. 1.0±0.4, n=6; p<0.0001) and a reduction in medullary tissue osmolality, while COX-1 did not change. Immunohistochemistry confirmed an increased COX-2 labeling associated with medullary interstitial cells. COX isoforms did not change in cortex/outer medulla after 24h BUO. In BUO kidneys, inner medullary AQP2 expression was reduced and this decrease was prevented by parecoxib. In the inner stripe of outer medulla NHE3 and BSC-1 were significantly reduced by BUO and this decrease was significantly attenuated by parecoxib. Immunohistochemistry for AQP2, NHE3 and BSC-1 confirmed the effect of parecoxib. Parecoxib had no significant effect on Na-K-ATPase alpha1 subunit, NaPi2 or AQP3. In conclusion, acute BUO leads to marked up-regulation of COX-2 in inner medulla and selective COX-2 inhibition, prevents dysregulation of AQP2, BSC-1 and NHE3 in response to BUO. These data indicate that COX-2 may be an important factor contributing to the impaired renal water and sodium handling in response to BUO.
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