Nitric Oxide Synthase and Coronary Vasospasm
نویسنده
چکیده
Nitric oxide (NO), the molecule of the year in 1995 and theme of the Nobel Prize in 1998, started its career as endothelium-derived relaxing factor (EDRF) almost 20 years ago.1 An unusual observation in the rabbit aorta, ie, the unexpected relaxation to acetylcholine only in preparations with endothelium, stimulated the scientific community because of its obvious physiological and clinical potential.2 The search for its identity left us with the surprising result that the answer was NO.3 This chemically unstable free radical and ancient mediator was fascinating not only because of its short half-life but also because it was the active component of all nitrovasodilators. Shortly thereafter, the enzyme nitric oxide synthase (NOS) was cloned and its substrate L-arginine identified.4,5 Thus, almost 100 years after the introduction of nitroglycerin in the treatment of angina pectoris, the endogenous nitrate was discovered, which, like its pharmacological counterpart, stimulated cGMP in vascular smooth muscle to cause vasodilatation.6
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Association between T-786C polymorphism of endothelial nitric oxide synthase gene and level of the vessel dilation factor in patients with coronary artery disease
Various polymorphisms on endothelial nitric oxide synthase (eNOs) gene cause reduced production of NO, the endothelial relaxing factor, and may accelerate the process of atherosclerosis. The study designed to investigate the frequency of T-786C polymorphism of the eNOs gene in patients suffering from coronary artery disease (CAD) in north-west of Iran. One hundred twenty subjects including 60 p...
متن کاملRetraction Note: Association between T-786C polymorphism of endothelial nitric oxide synthase gene and level of the vessel dilation factor in patients with coronary artery disease
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