Naturally occurring anthocyanin cyanidin-3-rutinoside possesses inherent vasorelaxant actions and prevents methylglyoxal-induced vascular dysfunction in rat aorta and mesenteric arterial bed

•Low concentrations of C3R promote endothelium-dependent vasodilation.•Intravenous administration of C3R induces hypotension in anesthetized rat.•Pre-treatment with MG enhances vascular contractility and impairs vasodilation.•C3R restores vascular functions (contraction/relaxation) in MG-treated vessels. Cyanidin-3-rutinoside (C3R) possesses anti-oxidant, anti-inflammatory and anti-glycation properties. Methylglyoxal (MG), a highly reactive dicarbonyl aldehyde by-product of glycolysis, is a precursor of advanced glycation end products and contributes to vascular dysfunction, particularly during hyperglycemia. We investigated the possible inherent vasoactivity of C3R, and its effectiveness against MG-induced vascular abnormalities in isolated blood vessel preparations from male Wistar Kyoto rat. C3R induced vasorelaxation concentration-dependently in aortic rings (92% maximum relaxation; EC50: 2.43±0.57μM) and in perfused-mesenteric arterial bed (61% maximum relaxation; EC50: 25.0±1.26μM) pre-contracted with noradrenaline (NA). The vasorelaxation actions of C3R were endothelium-dependent and mediated primarily via nitric oxide (NO) as evidenced by the absence of relaxation in endothelium-denuded preparations as well as in the presence of Nω-nitro-l-arginine, an inhibitor of NO synthase. Intravenous administration of C3R (15–25μmol/kg body weight) in anesthetized rats significantly reduced mean arterial blood pressure (11–23%). Pre-treatment with MG (500μM) potentiated the vasoconstriction elicited by NA and impaired vasorelaxation induced by acetylcholine that was fully restored to basal levels in the presence of C3R (3μM). Taken together, C3R exerts multiple benefits on the vasculature, complementing its potential as a candidate anti-glycation agent.