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ROLE OF NO IN CARDIOLOGICAL NUTRITION
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Abstract
Nitric Oxide (NO) which is produced in vascular endothelial cells, acts as an endocrine mediator, and has protective effects on the cardiovascular system through local vasodilation, angiogenesis, and growth inhibition smooth muscle and endothelial cell proliferation.
NO deficiency causes vascular endothelial dysfunction, compromised NO-mediated vasodilation, increased activation and adhesion of platelets and leukocytes; as well as the activation of cytokines that increase vascular permeability to oxidized lipoproteins and inflammatory mediators. OxLDLs impair the balance between constitutive eNOS and inflammatory factor iNOS in endothelial cells (ECs). Consequences lead to inhibition of protective mechanisms, such as eNOS function and self-protection, ultimately leading to endothelial cell apoptosis and subsequent endothelial dysfunction. The end result is that damage to the smooth muscle structure of the arterial wall, cell proliferation and the formation of atherosclerotic plaque.
Folic acid supplementation has antioxidant effects, increases endogenous NO synthesis through metabolism with BH4, so it has a protective effect on the arterial endothelium. Clinical trials have demonstrated that folic acid supplementation slightly lowers blood pressure, prevents stroke, and reduces cardiovascular events.
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Keywords
Nitric Oxide (NO, acid folic, vascular endothelial function, cardiovascular disease
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