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Tempol attenuates the development of hypertensive renal injury in Dahl salt-sensitive rats.

Hisaki R, Fujita H, Saito F, Kushiro T

Division of Cardiovascular Medicine, Surugadai Nihon University Hospital, Tokyo, Japan. rhisaki@med.nihon-u.ac.jp

BACKGROUND: Dahl salt-sensitive (DS) rats given a high-salt diet develop renal lesions that are virtually identical to those in human hypertensive nephrosclerosis and are associated with increased oxidative stress. This study looks at the effects of a superoxide scavenger in preventing of hypertensive renal damage in high-salt-treated DS rats. METHODS: The DS rats (n = 5 per group) were treated with 0.3% NaCl diets (LS), 8% NaCl diets (HS), and 8% NaCl diets plus 10 mmol/L tempol in drinking water (HS+T) for 5 weeks. Systolic blood pressure (SBP) was measured by the tail-cuff method. As markers of renal damage, we measured serum creatinine, creatinine clearance, histopathologic indices, and transforming growth factor-beta1 (TGF-beta1; a mediator for renal fibrosis) expression. In addition, 8-hydroxy-2'-deoxyguanosine (8-OHdG)-positive cells and expression of heme oxygenase-1 (HO-1) were quantified as markers of oxidative stress. RESULTS: We found that a high-salt diet (8% NaCl) led to the development of hypertension, increased oxidative stress in the renal tissue (8-OHdG immunoreactive staining and HO-1 protein expression), increased renal histopathologic damage (arteriosclerosis index, matrix score, and interstitial volume) accompanied by accumulation of TGF-beta1, and decreased creatinine clearance in the DS rats. These adverse effects of salt were prevented by the tempol supplementation. CONCLUSIONS: Histopathologic and biochemical findings indicate that, in the DS rat, salt-induced hypertensive nephropathy is associated with increased oxidative stress. Superoxide mimetic tempol can reduce this detrimental effect of salt feeding through TGF-beta1 suppression and consequently prevent the development of hypertension and hypertensive nephropathy.

Published 10 May 2005 in Am J Hypertens, 18(5): 707-13.
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