Resveratrol induces acute endothelium‐dependent renal vasodilation

Abstract

Resveratrol induces vasorelaxation in endothelium‐intact aortic strips through a nitric oxide (NO) mediated mechanism. We hypothesized resveratrol may act as an acute renal vasodilator through NO and/or prostanoid‐mediated mechanisms. In anesthetized rats, dose response experiments found 5.0 mg/kg 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). Heart rate (HR) and mean arterial pressure (MAP) remained unchanged. To test NO involvement, we administered 5.0 mg/kg resveratrol, before and after 10 mg/kg b.w. NOS inhibitor L‐NAME. L‐NAME increased MAP 38 mm Hg, decreased RBF by 39%, and doubled RVR. 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 role of endothelium‐derived prostanoids in resveratrol‐induced vasodilation, rats were treated with 10 mg/kg b.w. indomethacin. This treatment did not alter baselines or resveratrol‐induced vasodilation; and L‐NAME reduced resveratrol‐induced vasodilation by 44% from 0.50±0.09 to 0.28±0.06 ml/min/gkw (n=10 p<0.04) as before. We conclude acute intravenous resveratrol acts as an acute renal vasodilator, partially mediated by endothelial NO production but not by vasodilatory prostanoids. (NIH 5P01HL090550–04)