The Possible Implication oftrans-Resveratrol in the Cardioprotective Effects of Long-Term Moderate Wine Consumption

Abstract

trans-Resveratrol (t-RESV; 1-10 M), a phenolic component of wines, had no effect on phenylephrine-(PE; 1 M) and high KCl-(60 mM) induced contractions in endothelium-denuded rat aortic rings. However, it relaxed the contractile response produced by these vasoconstrictor agents in intact rat aorta. The vasorelaxing effects of t-RESV were completely inhibited by N G -nitro-L-arginine (L-NOARG; 0.1 mM) and methylene blue (10 M), but they were unaffected by atropine (10 M) and yohimbine (1 M). The reversal effect produced by L-NOARG was antagonized by L-arginine but not by D-arginine (0.1 mM). t-RESV (1-10 M) did not significantly modify rat aorta constitutive nitric-oxide synthase activity. However, this natural compound decreased NADH/NADPH oxidase activity in rat aortic homogenates. In addition, t-RESV (1-10 M) was ineffective in scavenging superoxide anions (O 2 . ) generated enzymatically by a hypoxanthine/xanthine oxidase (HX/XO) system and/or to inhibit XO. The above data demonstrate that the characteristic endothelium-dependent vasorelaxant effect of t-RESV in rat aorta seems to be caused by the inhibition of vascular NADH/ NADPH oxidase and the subsequent decrease of basal cellular O 2 . generation and, therefore, of NO biotransformation. Under the assumption that t-RESV exhibits a similar behavior in human blood vessels and bearing in mind that an overactivity of NADH/NADPH oxidase has been found in a number of cardiovascular pathologies, the results obtained in this work suggest that t-RESV could play an important role in the cardioprotective effects induced by the long-term moderate wine consumption.

Long-term resveratrol administration reduces metabolic disturbances and lowers blood pressure in obese Zucker rats

“…In the model of obese Zucker rats, as well as in subjects with insulin resistance, FFA are involved both in insulin resistance and in the inhibition of aortic eNOS activity through an oxidative mechanism [50,51]. The present results show that the chronic daily administration of resveratrol restores aortic expression of eNOS in obese Zucker rats, an effect which could explain the antihypertensive effects of this polyphenol in the insulin resistance model described, and which would be mediated by its antioxidant properties [15].…”

“…Beneficial cardiovascular properties of this polyphenol have been described previously [15,19,20]. Furthermore, the chronic administration of resveratrol enhances aortic eNOS expression in obese Zucker rats.…”

“…1) is a natural polyphenolic compound synthesized in a large number of plant species including some components of the human diet, such as mulberries, peanuts, grapes, and red wines. It is responsible for the beneficial effect of regular wine consumption in moderate amounts [15]. The positive effects of resveratrol in biological systems are wide-ranging.…”

“…It acts as a cancer chemoprevention agent [16], a powerful anti-inflammatory factor and an antioxidant agent [17,18]. Its cardiovascular properties, including inhibition of platelet aggregation and promotion of vasodilation by enhancing the production of NO [19] have also been described [15,20] and recent studies have reported its beneficial effects against ageing and metabolic diseases [21][22][23][24]. Resveratrol has been described as a potent activator of AMPK in several tissues and cell lines, i.e, HepG2 [24], C2C12 myotubes [25] neuronal cell lines and neurons [26].…”

Acute resveratrol supplementation improves flow-mediated dilatation in overweight/obese individuals with mildly elevated blood pressure

“…Improvements in FMD were correlated with a dose-related increase in plasma resveratrol concentrations. Whilst the FMD assessment does not reveal whether resveratrol is acting on the endothelium or on vascular smooth muscle to enhance vasodilatation, there is evidence to suggest that resveratrol can increase endothelium-derived NO bioavailability (14,(30)(31). Compared to placebo, our lowest dose (30mg) was shown to significantly improve FMD.…”