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Am J Physiol Renal Physiol 286: F509-F515, 2004. First published November 11, 2003; doi:10.1152/ajprenal.00253.2002
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Effect of UUO on D1aR expression reveals a link among dopamine, transforming growth factor-{beta}, and nitric oxide

Joshua M. Stern,1 Jie Chen,1 Randi B. Silver,2 Dix P. Poppas,1 E. Darracott Vaughan, Jr.,1 and Diane Felsen1

1The Institute for Pediatric Urology, Department of Urology, New York Presbyterian Children's Hospital-Weill Cornell Medical College, and 2Department of Physiology, Weill Medical College of Cornell University, New York, New York 10021

Submitted 15 July 2002 ; accepted in final form 26 October 2003

Interactions between transforming growth factor-{beta} (TGF-{beta}) and nitric oxide (NO) are important in the pathophysiology of unilateral ureteral obstruction (UUO). Dopamine (DA) is a vasoactive renal mediator active at the D1A receptor (D1AR), which has not been studied in UUO; therefore, we examined the interactions among DA, TGF-{beta}, and NO in UUO. In vivo, UUO was carried out in rats with or without concurrent treatment with 1D11, a monoclonal antibody to TGF-{beta}, for 14 days. In vitro, NRK-52E cells (normal rat kidney tubules) were treated with DA, and NO and TGF-{beta} release were examined. UUO resulted in a 70% decrease in the expression of renal D1AR, confirmed by both Western blot analysis and immunohistochemistry. 1D11 treatment restored expression to 60% of control values. DA treatment decreased NRK-52E release of TGF-{beta} by 80%; conversely, DA significantly increased NO release from NRK-52E cells. These results suggest that DA modulates the release of cytokines, which are involved in the fibrotic and apoptotic sequelae of UUO, and that these effects are independent of DA's known vasoactive properties.

kidney; obstructive uropathy; apoptosis; unilateral ureteral obstruction; D1A receptor


Address for reprint requests and other correspondence: D. Felsen, Weill Medical College, Dept. of Urology, Box 94, 1300 York Ave., New York, NY 10021 (E-mail: dfelsen{at}med.cornell.edu).




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