Abstract

Previous studies showed that chronic treatment with an antioxidant: vitamin C (vC) improves hypertension and sympathetic vasomotor hyperactivity in an Ang II‐dependent model of renovascular arterial hypertension. To test the hypothesis that oxidative stress is associated with NAD(P)H oxidase activation by Ang II, gene expressions of AT‐1 receptor (AT1R), NAD(P)H oxidase subunits (p47phox and gp91phox) and main antioxidant enzymes were evaluated in the renal cortex of 2 kidney‐1 clip model (2K1C, 6 weeks after clipping) rats before and after vC (150mg/kg/day). Gene expression of AT1R was elevated (51%) in the clipped kidney (CK) and reduced (47%) in the nonclipped kidney (NK) of 2K1C group. vC reduced AT1R expression only in the CK (31%). Elevated gene expression of p47phox and gp91phox was observed only in the CK of 2K‐1C group (184% and 132%, respectively) and vC produced no changes in these expressions. Gene expression of catalase was reduced in the CK (70%) and NK (83%) of 2K1C rats. vC increased gene expression of glutathione peroxidase (GPx) in the CK (185%) and NK (212%) of 2K1C. The present study suggests that renal oxidative stress may be related to elevated AT1R and NAD(P)H oxidase subunits gene expression in the CK of 2K1C rats and vitC treatment may produce beneficial effects by AT1R downregulation in the CK and increase in GPx gene expression in the kidneys of 2K1C rats.Supported by FAPESP (07/56925‐1)

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