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1 Physical-Chemistry, School of Pharmacy and Biochemistry, University of Buenos Aires, Buenos Aires, Buenos Aires, Argentina
2 Laboratory of Experimental Medicine, Hospital Aleman, Buenos Aires, Buenos Aires, Argentina
3 Physiology, Ponce School of Medicine, Ponce, Ponce, Puerto Rico
4 Experimental Nephrology, Institute of Cardiovascular Research, School of Medicine, University of Buenos Aires, Buenos Aires, Buenos Aires, Argentina
* To whom correspondence should be addressed. E-mail: felinserra{at}yahoo.com.ar.
Mitochondrial dysfunction is associated with cardiovascular damage; however, data on a possible
association with kidney damage are scarce. Here we aimed at investigating whether a) kidney impairment is related to mitochondrial dysfunction, and b) angiotensin II blockade, as compared to Ca2+-channel blockade, can reverse potential mitochondrial changes in hypertension. Eight-weekold male spontaneously hypertensive rats (SHR) received water containing losartan (40 mg/kg/day, SHR+Los), Amlodipine (3 mg/kg/day, SHR+Amlo), or no-additions (SHR) for 6-months. Wistar-Kyoto rats (WKY) were normotensive controls. Glomerular and tubulointerstitial damage, systolic blood pressure, and proteinuria were higher, and creatinine clearance was lower in SHR versus SHR+Los and WKY. In SHR+Amlo, blood pressure was similar to WKY, kidney function was similar to SHR, and renal lesions were lower than in SHR, but higher than in SHR+Los. In kidney mitochondria from SHR and SHR+Amlo, membrane potential, nitric oxide synthase, Mnsuperoxide dismutase and cytochrome oxidase activities, and uncoupling protein-2 content were lower than in SHR+Los and WKY. In SHR and SHR+Amlo, mitochondrial hydrogen peroxide production was higher than in SHR+Los and WKY. Renal glutathione content was higher in SHR and SHR+Amlo relative to SHR+Los and WKY, but in the latter groups glutathione was relatively more reduced. Tubulointerstitial 
-smooth muscle actin labeling was inversely related to Mnsuperoxide dismutase activity and UCP2 content. These findings suggest that oxidant stress is associated with renal mitochondrial dysfunction in SHR. The mitochondrial-antioxidant actions of losartan may be an additional or alternative way to explain some of the beneficial effects of AT1-receptor antagonists.
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