title: L-Arginine in coronary atherosclerosis.
abstract: Nitric oxide is formed from the N-guanido terminal of the amino acid L-arginine and from molecular oxygen by nitric oxide synthase enzymes. L-arginine administration improves the coronary blood flow response to acetylcholine in patients with normal coronary arteries and hypercholesterolemia, reverses the defective endothelium-dependent vasodilation associated with an elevated plasma low-density lipoprotein level or hypercholesterolemia, dilates coronary epicardial arteries and stenoses, enhances nitric oxide generation, and inhibits lesion formation after balloon angioplasty. Stimulation of endogenous nitric oxide production could inhibit atherogenesis, and therefore may be of benefit in patients with risk factors for atherosclerosis.
authors.affiliation: Cardiology Unit, Hippokration Hospital, Athens University Medical School, Athens, Greece.
authors.forename: C
authors.initials: C
authors.lastname: Tentolouris
authors.forename: D
authors.initials: D
authors.lastname: Tousoulis
authors.forename: G
authors.initials: G
authors.lastname: Goumas
authors.forename: C
authors.initials: C
authors.lastname: Stefanadis
authors.forename: G
authors.initials: G
authors.lastname: Davies
authors.forename: P
authors.initials: P
authors.lastname: Toutouzas
mesh_terms: D001120:Arginine / Q000502:physiology*; D003324:Coronary Artery Disease / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D006937:Hypercholesterolemia / Q000503:physiopathology; D012307:Risk Factors; D012907:Smoking; D014664:Vasodilation / Q000502:physiology
chemical_list: D001120:Arginine