Resveratrol is suggested to have beneficial cardiovascular and renoprotective effects. Resveratrol increases endothelial nitric oxide synthase (eNOS) expression and nitric oxide (NO) synthesis. We hypothesized resveratrol acts as an acute renal vasodilator, mediated through increased NO production and scavenging of reactive oxygen species (ROS). In anesthetized rats, we found 5.0 mg/kg b.w. resveratrol increased renal blood flow (RBF) by 8% (from 6.98±0.42 to 7.54±0.17 ml/min/gkw n=8 p<0.002), and decreased renal vascular resistance (RVR) by 18% from 15.00±1.65 to 12.32±1.20 ARU (p<0.002). To test the participation of NO, we administered 5.0 mg/kg b.w. resveratrol, before and after 10 mg/kg b.w. of the NOS inhibitor, L-NAME. L-NAME reduced the increase in RBF to resveratrol by 54% (from 0.59±0.05 to 0.27±0.06 ml/min/gkw, n=10 p<0.001). To test the participation of ROS, we gave 5.0 mg/kg b.w. resveratrol before and after 1 mg/kg b.w. tempol, a superoxide dismutase mimetic. Resveratrol increased RBF 7.6% (from 5.91±0.32 to 6.36±0.12 ml/min/gkw n=7 p<0.001) and decreased RVR 19% (from 18.83±1.37 to 15.27±1.37 ARU). Tempol blocked resveratrol-induced increase in RBF (from 0.45±0.12 to 0.10±0.05 ml/min/gkw, n=7 p<0.03) and the decrease in RVR post-tempol was 44% of the control response (3.56±0.34 vs. 1.57±0.21 ARU n=7 p<0.006). We also tested the role of endothelium-derived prostanoids. Two days of 10 mg/kg b.w. indomethacin pretreatment did not alter basal blood pressure or RBF. Resveratrol-induced vasodilation remained unaffected. We conclude intravenous resveratrol acts as an acute renal vasodilator, partially mediated by increased NO production/NO bioavailability and superoxide scavenging, but not by inducing vasodilatory cyclooxygenase products.