Oxidative and nitrosative stress have been implicated in high sodium diet (HSD)-related hypertensive renal injury. In the present study we investigated AT2R-mediated renoprotection in obese Zucker rats fed HSD. Obese Zucker rats were fed normal sodium-diet (NSD) or HSD 4%, for 14 days, with/without AT2R agonist C21, delivered subcutaneously via osmotic pump, 1 mg/kg/day. Compared to NSD controls, HSD rats exhibited increase in cortical NADPH oxidase activity, urinary H2O2 and 8-isoprostanes, which were associated with severe glomerulosclerosis, interstitial fibrosis, decline in estimated glomerular filtration rate (eGFR), and an increase in urinary leak and activity of N-acetyl-β-D-glucosaminidase, a lysosomal enzyme and a marker of tubular damage. These changes were improved by C21 treatment. Cortical expression of endothelial nitric oxide synthase (eNOS), p-eNOS (Ser1177) and plasma nitrites were reduced after HSD intake while nitrosative stress (3-nitrotyrosine) and enzymatic defense (superoxide dismutase-to-catalase activity) remained unaltered. Albeit, C21 preserved plasma nitrites in HSD-fed OZR. C21 treatment reduced protein-to-creatinine (uPcr), albumin-to-creatinine (uAcr) as well as fractional excretion of protein (FEpro) and albumin (FEalb) in HSD-fed OZR, which is independent of changes in protein recycling receptors, megalin and cubilin. HSD intake also altered renal excretory and reabsorptive capacity as evident by elevated plasma urea nitrogen-to-creatinine (UN-to-cr) and fractional excretion of urea nitrogen (FEUN), and reduced urine-to-plasma creatinine (UPcr), which were modestly, but insignificantly, improved by C21 treatment. Together results demonstrate that AT2R activation protects against HSD-induced kidney damage in obesity plausibly by reducing NOX activity and rescuing nitrites.