Endothelial dysfunction, characterized by a disturbed vascular NO metabolism, represents a key point in atherogenesis. Modern antiatherogenic therapies improve NO availability within the endothelium. As L-arginine acts as the substrate of endothelial nitric oxide synthase (eNOS), arginine supplementation can enhance NO formation. Actually, L-arginine at appropriate dosage (6–8 g/day) improves endothelial function and lowers blood pressure. However, beneficial effects can only be expected in individuals with pronounced endothelial dysfunction and/or individuals with an absolute (patients with hemodialysis) or relative (patients with elevated ADMA levels) arginine deficiency. Whether L-arginine delays progression of atherosclerotic lesions and lowers cardiovascular morbidity and mortality is unknown.
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