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Am J Physiol Renal Physiol (October 10, 2006). doi:10.1152/ajprenal.00252.2006
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Submitted on July 5, 2006
Accepted on October 2, 2006

Proximal Tubule Microvilli Remodeling and Albuminuria in the Ren2 Transgenic Rat

Melvin R Hayden1, Nazif Chowdhury2, Shawna A Cooper2, Adam Whaley-Connell3, Javad Habibi4, Lauren Witte2, Charles E Wiedmeyer5, Camila M Manrique2, Guido Lastra2, Carlos M Ferrario6, Craig S. Stump7, and James R. Sowers8*

1 Internal Medicine, University of Missouri School of Medicine, 65212, Missouri, United States; Division of Endocrinology, United States
2 Internal Medicine, University of Missouri School of Medicine, 65212, Missouri, United States
3 Internal Medicine, University of Missouri School of Medicine, 65212, Missouri, United States; Division of Nephrology, Columbia, Missouri, United States
4 Internal Medicine, University of Missouri School of Medicine, Columbia, Missouri, United States
5 University of Missouri College of Veterinary Medicine, Columbia, Missouri, United States
6 Hypertension Center, Wake Forest University School of Medicine, Winston-Salem, North Carolina, United States
7 Medicine-Endocrinology, University of Missouri-Columbia, Columbia, Missouri, United States
8 Department of Internal Medicine, University of Missouri, Columbia, Missouri, United States

* To whom correspondence should be addressed. E-mail: sowersj{at}health.missouri.edu.

TG(mRen2)27 (Ren2) transgenic rats overexpress the mouse renin gene with subsequent elevated tissue Ang-II, hypertension, and nephropathy. The proximal tubule cell (PTC) is responsible for the reabsorption of 5-8 grams of glomerular filtered albumin (Alb) each day. Excess filtered albumin may contribute to PTC damage and tubulointerstitial disease. This investigation examined the role of angiotensin-II (Ang-II) induced oxidative stress in PTC structural remodeling; whether such changes could be modified with in vivo treatment with Ang type 1 receptor (AT1R) blockade (valsartan) or superoxide dismutase/catalase mimetic (tempol). Male Ren2 (6-7 week old) and age-matched Sprague-Dawley (SD) rats were treated with valsartan (Ren2-V; 30 mg/kg), tempol (Ren2-T; 1 mmol/L), or placebo for three weeks. Systolic blood pressure (SBP), albuminuria, n-acetyl-{beta}-d-glucosaminidase (beta-NAG), kidney tissue malondialdehyde (MDA) were measured and PTC microvilli structure assessed using 60K transmission electron microscopy (TEM) images. There were significant differences in SBP, albuminuria, lipid peroxidation (MDA and Nitrotyrosine staining), and PTC structure in Ren2 versus SD rats (each p <0.05). Increased mean diameter of PTC microvilli in the Ren2-C (p <0.05) correlated strongly with albuminuria (r2 = 0.83) and moderately with MDA (r2 = 0.49), and there was an increase in the ratio of abnormal forms of microvilli in Ren2 rats when compared to SDC (p <0.05). AT1R blockade, but not tempol treatment, abrogated albuminuria and beta-NAG; both therapies corrected abnormalities in oxidative stress and PTC microvilli remodeling. These data indicate that PTC structural damage in the Ren2 rat is related to oxidative stress response to Ang-II and/or albuminuria.




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