No abstract

Several reports suggest that consumption of red wine is associated with a lower risk of stroke. We investigated the chronic effect of red wine polyphenols (RWP) on the functional and structural characteristics of cerebral arterioles in chronic hypertension, which is an important risk factor of stroke. Spontaneous hypertensive rats (SHR) were treated with RWP extract (100 mg/kg/day in drinking water) for 10 weeks. We measured the effect of agonist- and hypotension-induced changes in internal diameter of cerebral arterioles using an open cranial window technique. Wall mechanical parameters were determined in deactivated cerebral arterioles. The activity of antioxidant enzymes in plasma was determined. Adenosine diphosphate-induced vasodilatation was decreased by 48% in SHR and normalized in SHR treated with RWP. RWP had no effect on hypotension-induced dilatation. RWP decreased the wall thickness/external diameter ratio by 13% and significantly shifted the stress-strain relationship of the arteriole wall to the left. There was a decrease in glutathione-S-transferase and glutathione peroxidase after treatment of RWP in SHR. In summary, chronic oral administration of RWP to SHR improved endothelium-dependent dilatation, normalized wall stress and diameter, and altered the systemic antioxidant state. These effects of RWP could be useful in the prevention of stroke in hypertensive patients.

Incubation of aortic rings in a culture medium produces phenomena similar to those observed with aging, i.e. oxidative stress and inflammation leading to increased nitric oxide (NO)‐mediated dilation and decreased arterial sensitivity to vasoconstrictor agents. We evaluated whether melatonin protects aortic rings from such a decrease in vasoreactivity. Two concentrations of melatonin were used: 10−8 m, EC50 for vascular MT1–MT2 receptors, and 10−5 m, reported as anti‐oxidant. Anti‐oxidant capacity, inducible nitric oxide synthase (iNOS) expression and isometric contraction of thoracic aorta rings (Wistar rats) evoked by norepinephrine (NE) were assessed. Three days of incubation of aortic rings induced iNOS expression and a fall in NE‐evoked contraction. When melatonin was added to the organ bath, it (10−5 m) increased (+96%, P < 0.05), but did not restore (compared with freshly isolated rings) NE‐evoked contraction. Three days of treatment with melatonin increased (10−8 m, +99%) or restored (10−5 m, +216%) NE‐evoked contraction (compared with freshly isolated rings). The beneficial effects of 10−8 and 10−5 m melatonin on NE‐evoked contraction were abolished in the presence of luzindole (2 × 10−6 m, a melatonin receptor antagonist). The incubation‐induced increase in iNOS expression was reduced following 3 days of melatonin administration (10−8 and 10−5 m). Melatonin (10−5 m) increased catalase activity (6550 ± 256, P < 0.05 vs. nontreated fresh aortic rings 5554 ± 444 nmol min−1 mg protein−1). In conclusion, melatonin counteracts the incubation‐induced loss of agonist‐evoked contraction of aortic rings by a specific receptor‐mediated phenomenon involving iNOS expression; at higher melatonin concentrations, an anti‐oxidant effect is probably also involved.