Red wine polyphenols have been reported to exert beneficial effects in preventing cardiovascular diseases but their molecular mechanisms of hemodynamic effects on functional cardiovascular and renal changes were studied much less. The review is focused on in vitro as well as in
vivo effects of red wine extract containing polyphenolic compounds
(Provinols™) on cardiovascular systems and kidney in relation to the molecular and biochemical mechanisms of these compounds. This review provides the evidence that Provinols™ is able to produce ex vivo
endothelium-dependent relaxation as a result of enhanced NO synthesis. Administration of Provinols™ partially prevents the development of hypertension during NO deficiency and accelerates the decrease of blood pressure in already established hypertension. The effects of Provinols™ include prevention and/or attenuation of myocardial fibrosis, reduction of aortic wall thickening and improvement of vascular functions. These functional and structural alterations are associated with significant augmentation of NO production, seen as the increase of NO synthase activity and eNOS protein expression. Moreover, it has been documented that Provinols™ decreased the oxidative stress within the cardiovascular system and kidney.
Present study investigated the effect of red wine polyphenolic compounds (ProvinolsTM) on blood pressure (BP), nitric oxide synthase (NOS) activity and vascular function in Wistar-Kyoto (WKY) rats exposed to chronic social stress produced by crowding. Adult male rats were divided into four groups: control (480 cm2/rat), ProvinolsTM-treated (20 mg/kg/day, 480 cm2/rat), crowded (200 cm2/rat) and crowded treated with Provinols
TM (20 mg/kg/day, 200 cm2/rat) for 8 weeks. No differences in BP were observed among the groups at the end of experiment, however, reduced BP was observed in ProvinolsTM-treated rats after 3 weeks of treatment. NOS activity in the aorta was significantly elevated in crowded rats, while ProvinolsTM alone had no effect on nitric oxide (NO) production. Acetylcholine-induced relaxation of the femoral artery was significantly improved in stressed and ProvinolsTM-treated rats vs. control, without significant changes in their noradrenaline-induced vasoconstriction. Interestingly, ProvinolsTM blunted the elevation of NO production and vasorelaxation during crowding. Increased endothelium-dependent vasorelaxation and NO synthesis in crowded rats may represent the adaptation mechanisms, resulting in unaltered blood pressure in stress-exposed normotensive rats. This study further demonstrated that elevated release of NO during chronic stress may be prevented by ProvinolsTM. Thus, Provino TM might maintain equilibrium between endothelium-derived vasoconstrictor and vasodilator factors in stress.