| Resveratrol (3, 4', 5-trihydroxystilbene) is a phytoalexin polyphenolic compound naturally produced by plants in response to fungal infection or abiotic stresses, such as heavy metal ions and ultraviolet light (UV). Resveratrol occurs in many kinds of plants such as grapes, peanuts, cranberries as well as in wine especially red wine. Resveratrol exhibits a wide range of biological effects, including cancer chemoprevention, antioxidative, antiplatelet, antifungal, anti-inflammatory, phytoestrogentic, and cardioprotective activities. Since resveratrol is found in high concentration in some red wine, interest in this compound has expanded. Numerous epidemiologic studies have showed an inverse correlation between red wine consumption and incidence of cardiovascular disease. Several recent studies determined the cardioprotective abilities of resveratrol. Both in acute and in chronic models, resveratrol protects the cardiovascular system against ischemic-reperfusion injury, promotes vasorelaxation, protects and maintains the intact endothelium, exhibits antiatherosclerotic properties, inhibits the low-density lipoprotein oxidation, suppresses the platelet aggregation and exhibits estrogen like action. Additionally, resveratrol can induce vasorelaxations which may relate to inhibition of Ca2+ influx and Ca2+ release from intracellular stores, and the relaxing response of resveratrol is endothelium-dependent in part [9]. Thus resveratrol may have a potential clinical value in the treatment of cardiovascular disease as an alternative medicine. It is well known that baroreflex is a major way to modulate blood pressure. The effects of resveratrol on carotid sinus baroreceptor activity and baroreflex have not been reported yet; the goals of the present research were to observe these effects of resveratrol.1 Resveratrol inhibits carotid sinus baroreflex in anesthetized male ratsObjective: To study the effects of resveratrol on carotid sinus baroreflex (CSB).Methods: The functional curve of carotid sinus baroreflex was measured by recording the changes of arterial pressure in 36 anesthetized male rats with isolated perfusing carotid sinus.Results: (1) Resveratrol (30, 60 and 120μmol.L-1) inhibited CSB, which shifted the functional curve of the baroreflex to the right and upward, with a marked decrease in peak slope (PS) and reflex decrease (RD) in blood pressure in a concentration-dependent manner. PS decreased from 0.46±0.01 to 0.39±0.02, 0.32±0.02, 0.26±0.01 respectively. RD decreased from (47.00±2.76) mmHg to (39.33±1.86), (33.00±1.41), (28.00±1.67) mmHg; threshold pressure (TP) increased from (65.80±1.51) mmHg to (70.32±2.33), (76.18±1.68), (83.05±1.73) mmHg; equilibrium pressure (EP) increased from (93.60±0.52) mmHg to (95.95±0.52), (97.79±0.55), (99.63±0.82) mmHg; saturation pressure (SP) increased from (187.50±1.87) mmHg to (191.00±2.37), (197.33±1.63), (203.67±2.50) mmHg respectively. (2)Pretreatment with Nω-nitro-L-arginine methyl ester (L-NAME, 100μmol.L-1), an inhibitor of nitric oxide synthase (NOS), eliminated the inhibitory effect of resveratrol. (3) Pretreatment with Bay K8644 (an agonist of L-type calcium channel, 500 nmol.L-1) abolished the effect of resveratrol on CSB. (4) A potent inhibitor of tyrosine phosphatase (sodium orthovanadate, 1 mmol.L-1) did not influence the effect of resveratrol on CSB.Conclusion: Resveratrol inhibits carotid baroreflex, which is mediated by the locally released NO and decreased calcium influx.2 Resveratrol inhibits carotid sinus baroreceptor activity in anesthetized male ratsObjective: To study the effect of resveratrol on carotid baroreceptor activity (CBA).Methods: The functional curve of carotid baroreceptor (FCCB) was constructed and the functional parameters of carotid baroreceptor were measured by recording sinus nerve afferent discharge in 36 anesthetized male rats with perfused isolated carotid sinus.Results: (1) Resveratrol (30, 60 and 120μmol.L-1) inhibits CBA, which shifted FCCB to the right and downward. There was a marked decrease in peak slope (PS) and peak integral value (PIV) of carotid sinus nerve charge in a concentration-dependent manner. PS decreased from (3.00±0.06)%mmHg-1 to (2.58±0.11), (2.37±0.09), (2.05±0.07)% mmHg-1 respectively. PIV decreased from (329.00±3.90)% to(279.67±1.63), (243.50±3.73), (214.67±3.50)% respectively; threshold pressure (TP) increased from (45.13±1.96) mmHg to (50.40±1.09), (58.14±4.60), (68.17±3.68) mmHg; saturation pressure (SP) increased from (157.50±1.87) mmHg to (165.00±1.41), (171.50±2.07), (184.50±1.05) mmHg.(2) Pretreatment with Nω-nitro-L-arginine methyl ester (L-NAME, 100μmol.L-1), an inhibitor of nitric oxide synthase (NOS), eliminate the inhibitory effect of resveratrol. (3) Pretreatment with Bay K8644 (an agonist of L-type calcium channel, 500 nmol.L-1) abolished the effect of resveratrol on CBA. (4) A potent inhibitor of tyrosine phosphatase (sodium orthovanadate, 1 mmol.L-1) did not influence the effect of resveratrol on CBA.Conclusion: Resveratrol inhibits carotid baroreceptor activity, which is mediated by the locally released NO and decreased calcium influx.
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