Background/Aim: We examined the influence of chronic treatment with angiotensin-(1–7) [Ang-(1–7)] on renox (renal NADPH oxidase, NOX-4) and the development of renal dysfunction in streptozotocin-treated spontaneously hypertensive rats (diabetic SHR). Methods: Mean arterial pressure, urinary protein and vascular responsiveness of the isolated renal artery to vasoactive agonists were studied in vehicle- or Ang-(1–7)-treated SHR and diabetic SHR. Results: Ang-(1–7) decreased the elevated levels of renal NADPH oxidase (NOX) activity and attenuated the activation of NOX-4 gene expression in the diabetic SHR kidney. Ang-(1–7) treatment increased sodium excretion but did not affect mean arterial pressure in diabetic SHR. There was a significant increase in urinary protein (266 ± 22 mg/24 h) in the diabetic compared to control SHR (112 ± 13 mg/24 h) and treatment of diabetic SHR with Ang-(1–7) reduced the degree of proteinuria (185 ± 23 mg/24 h, p < 0.05). Ang-(1–7) treatment also attenuated the diabetes-induced increase in renal vascular responsiveness to endothelin-1, norepinephrine, and angiotensin II in SHR, but significantly increased the vasodilation of the renal artery of SHR and diabetic SHR to the vasodilator agonists. Conclusion: These results suggest that treatment with Ang-(1–7) constitutes a potential therapeutic strategy to alleviate NOX-mediated oxidative stress and to reduce renal dysfunction in diabetic hypertensive rats.

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