Vitis vinifera is commonly known as the classic wine grape. Grapes and theirjuices are high in flavonoids, which are believed to give red wine its cardiovascular protective qualities. Research has shown that grape products, such as grapejuice and red wine, increase NO release from platelets, and decrease platelet aggregation and superoxide production.55 More specifically, research on a constituent of grape skins and seeds known as resveratrol has produced effects on NO. Resveratrol has been demonstrated to have estrogen-like activity and antioxidant, antiplatelet, anti-inflammatory, and anticarcinogenic properties. Studies indicate that resveratrol up-regulates the gene expression of endothelial NOS with a resulting increase in NO levels.56
The root of American ginseng (Panax quinquefolius) is often used as a supplement because of its adaptogenic properties. It is often used for immune modulation and stress resistance, to treat diabetes and hormone imbalances, and as a stimulant. Studies have indicated that ginseng stimulates NO release in vitro.57
Cynara scolymus (or Cynara cardunculus) is commonly known as the artichoke. This plant lowers lipids, has antioxidant properties, and calms the digestive system. Luteolin and cy-naroside are two flavonoids found in artichoke, which affect NO. These flavonoids increase NOS expression in endothelial cells.58
Quercetin is a citrus bioflavonoid used for treating conditions such as atherosclerosis, coronary heart disease, hypercholesterolemia, vascular insufficiency, diabetes, and allergies. Many studies on rats with diabetes have demonstrated that quercetin increases NO availability and induces vasorelaxation via the endothelial NOS pathway.59,60
Dehydroepiandrosterone (DHEA) is an androgen made in the adrenal glands, liver, and testes. This androgen is converted to androstenedione, which is metabolized to other androgens and estrogen. Studies have suggested that DHEA decreases atherosclerosis via a NO-dependent system; researchers have measured increases in NO with DHEA supplementation. This may be partially explained by DHEA's conversion to estrogen.61
Melatonin has been shown to decrease mitochondrial NOS induction from bacteria as a result of lipopolysaccharides. It has been suggested that age-related decreases in melatonin may be correlated with the mitochondrial damage that increases with aging. However, this may protect the body from oxidative damage because large amounts of NO are produced in sepsis and shock.62
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