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Articles in PresS, published online ahead of print May 15, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00098.2002
Submitted on February 19, 2002
Accepted on May 11, 2002
1 Department of Physiology, Medical College of Wisconsin, Milwaukee, WI, USA
2 Genzyme Corp., Framingham, MA, USA
* To whom correspondence should be addressed. E-mail: rroman{at}mcw.edu.
This study examined the role of transforming growth factor-beta (TGF-ß) in the development of hypertension and renal disease in 9 week old male Dahl S rats fed an 8% NaCl diet for 3 weeks. The rats received i.p. injections of a control or an anti-TGF-ß antibody (anti-TGF-ß Ab) every other day for two weeks. Mean arterial pressure (MAP) was significantly lower in Dahl S rats treated with anti-TGF-ß Ab (177 ± 3 mm Hg, n=12) than in control rats (190 ± 4 mm Hg, n=17). Anti-TGF-ß Ab therapy also reduced proteinuria from 226 ± 20 mg/day to 154 ± 16 mg/day. Renal blood flow, cortical blood flow and creatinine clearance were not significantly different in control and treated rats; however, medullary blood flow (MBF) was 3-fold higher in the treated rats than in the controls. Despite the reduction in proteinuria, the degree of glomerulosclerosis and renal hypertrophy were similar in control and anti-TGF-ß Ab treated rats. Renal levels of TGF-ß1 and ß2, 
-actin, type III collagen and fibronectin mRNA decreased in rats treated with anti-TGF-ß Ab. To examine whether an earlier intervention with anti-TGF-ß Ab would confer additional renoprotection, these studies were repeated in a group of 6 week old Dahl S rats. Anti-TGF-ß Ab therapy significantly reduced blood pressure, proteinuria and the degree of glomerulosclerosis and renal medullary fibrosis in this group of rats. The results indicate that anti-TGF-ß Ab therapy reduces blood pressure, proteinuria and renal injury associated with hypertension.
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