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Background  Kinin B 1  receptor (B 1 R) is induced by the oxidative stress in models of diabetes mellitus. This study aims at determining whether B 1 R activation could perpetuate the oxidative stress which leads to diabetic complications.    Methods and Findings  Young Sprague-Dawley rats were fed with 10% D-Glucose or tap water (controls) for 8–12 weeks. A selective B 1 R antagonist (SSR240612) was administered acutely (3–30 mg/kg) or daily for a period of 7 days (10 mg/kg) and the impact was measured on systolic blood pressure, allodynia, protein and/or mRNA B 1 R expression, aortic superoxide anion (O 2   •− ) production and expression of superoxide dismutase (MnSOD) and catalase. SSR240612 reduced dose-dependently (3–30 mg/kg) high blood pressure in 12-week glucose-fed rats, but had no effect in controls. Eight-week glucose-fed rats exhibited insulin resistance (HOMA index), hypertension, tactile and cold allodynia and significant increases of plasma levels of glucose and insulin. This was associated with higher aortic levels of O 2   •− , NADPH oxidase activity, MnSOD and catalase expression. All these abnormalities including B 1 R overexpression (spinal cord, aorta, liver and gastrocnemius muscle) were normalized by the prolonged treatment with SSR240612. The production of O 2   •−  in the aorta of glucose-fed rats was also measured in the presence and absence of inhibitors (10–100 µM) of NADPH oxidase (apocynin), xanthine oxidase (allopurinol) or nitric oxide synthase (L-NAME) with and without Sar[D-Phe 8 ]des-Arg 9 -BK (20 µM; B 1 R agonist). Data show that the greater aortic O 2   •−  production induced by the B 1 R agonist was blocked only by apocynin.    Conclusions  Activation of kinin B 1 R increased O 2   •−  through the activation of NADPH oxidase in the vasculature. Prolonged blockade of B 1 R restored cardiovascular, sensory and metabolic abnormalities by reducing oxidative stress and B 1 R gene expression in this model.

Kinin B1 Receptor Enhances the Oxidative Stress in a Rat Model of Insulin Resistance: Outcome in Hypertension, Allodynia and Metabolic Complications