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Am J Physiol Regul Integr Comp Physiol (January 23, 2003). doi:10.1152/ajpregu.00257.2002
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Submitted on May 10, 2002
Accepted on January 8, 2003

Gene expression reveals vulnerability to oxidative stess and interstitial fibrosis of the renal outer medulla to non-hypertensive elevations of angiotensin II

Baozhi Yuan1, Mingyu Liang1, Zhizhang Yang1, Elizabeth Rute1, Norman Taylor1, Michael Olivier1, and Allen W Cowley, Jr.1*

1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA

* To whom correspondence should be addressed. E-mail: cowley{at}mcw.edu.

The present study was designed to determine whether non-hypertensive elevations of plasma Ang II would modify the expression of genes involved in renal injury that could influence oxidative stress and extracellular matrix formation in the renal medulla using microarray, Northern and Western blot techniques. Sprague-Dawley rats were infused i.v. with either AngII (5 ng/kg/min) or vehicle for seven days (N=6/group). Mean arterial pressure (MAP) averaged 110±0.6 during the control period and 113+0.4 mmHg following Ang II. The mRNA of 1,751 genes (~80% of all currently known rat genes) that was differentially expressed (Ang II vs saline) in renal outer and inner medulla was determined. The results of 12 hybridizations indicated that in response to AngII, 11 genes were up-regulated and 25 down-regulated in the outer medulla, while 11 were up-regulated and 13 down-regulated in the inner medulla. These differentially expressed genes, most of which were not known previously to be affected by AngII in the renal medulla, were found to group into 8 physiological pathways known to influence renal injury and kidney function. Particularly, expression of several genes would be expected to increase oxidative stress and interstitial fibrosis in the outer medulla. Western blot analyses confirmed increased expression of TGF-{beta}1 and collagen type IV proteins in the outer medulla. Results demonstrate that non-hypertensive elevations of plasma Ang II can significantly alter the expression of a variety of genes in the renal outer medulla and suggested the vulnerability of the renal outer medulla to the injurious effect of Ang II.




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