Resveratrol

Research on resveratrol done in vitro (in the test tube and outside a living organism) has found that it produces some effects that have potential protective functions related to cardiovascular problems. These biological effects include inhibition of platelet aggregation, stimulation of endothelial nitric oxide synthase activity, inhibition of vascular cell adhesion molecule expression, and inhibition of vascular smooth muscle cell proliferation. The concentrations of resveratrol used in these studies are usually much higher than those that have been measured in humans who have orally consumed resveratrol. Thus, although the research findings are positive, their application to human intake is still being researched.

One of the activities of resveratrol related to the prevention of cardiovascular disease is inhibition of platelet aggregation. Platelets, also known as thrombocytes, are small disc-shaped cells that circulate in the blood of mammals. Platelet aggregation involves the clustering of platelets that contributes to the formation of a thrombus or clot, which can obstruct a coronary artery, resulting in a heart attack. A study done by researchers at New York Medical College in 2000 found that resveratrol blocks aggregation of platelets. It does so by blocking receptor-mediated signaling events among platelets. However, the researchers found that while resveratrol had significant inhibiting activity of washed platelets, it had poor results in decreasing platelet aggregation in whole blood. They indicated that resveratrol’s activity is weakened or masked in circulation in the blood.

Resveratrol has also been observed to stimulate endothelial nitric oxide synthase (eNOS) activity in cultured endothelial cells, another activity related to heart disease prevention. eNOS is an enzyme that is responsible for producing nitric oxide. Nitric oxide is antiatherogenic, meaning that it helps prevent clogging of arteries. High nitric oxide levels in the endothelium, the innermost layer of cells lining artery walls, increases and protects these artery walls. Nitric oxide plays a part in maintaining arterial relaxation; when this function is impaired, it is associated with increased risk of cardiovascular disease. Wallerath and colleagues in 2003 tested the effects of resveratrol on eNOS expression in human endothelial cells. They found that eNOS protein expression and eNOS-derived nitric oxide production were increased after long-term incubation with resveratrol. Resveratrol also increased the production of bioactive nitric oxide after short-term incubation. They concluded that this activity, along with others, may contribute to the cardiovascular protective effects attributed to resveratrol. In another study in 2005, Klinge and colleagues demonstrated that resveratrol stimulated eNOS activity. They also indicated that the effects of resveratrol may be mediated through rapid activation of estrogen receptor signaling in endothelial cells.