Exercise and cardiovascular health: get active to "AKTivate" your endothelial nitric oxide synthase.
نویسندگان
چکیده
Epidemiological studies have clearly documented that regular physical exercise promotes cardiovascular health and reduces the risk in patients with established coronary heart disease.1,2 The mechanisms mediating the atheroprotective effects of exercise are not clearly defined. Multiple possible mediators have been suggested, including various physiological adaptations, altered autonomic function, and metabolic adjustments. Regular physical activity is associated with favorable modification of cardiovascular risk factors such as hypertension, diabetes, obesity, and hypercholesterolemia.3 However, the beneficial effects of regular physical activity cannot be accounted for solely by reduction of risk factors, because the association with reduced mortality is independent of other coronary risk factors.3 In recent years, it has become apparent that exercise directly affects the functional activity of the vascular endothelium.4 By increasing the mechanical shear forces on the luminal surface of the endothelial monolayer, exercise-induced increases in blood flow enhance the vasodilatory capacity of the arteries in animal models and in patients.4,5 The endothelium not only plays a pivotal role in controlling vascular tone but exerts several important antiatherosclerotic functions, such as preventing platelets and inflammatory cells from adhering to the vascular surface. Indeed, the functional integrity of the endothelium to respond to increased blood flow is the major independent predictor of atherosclerotic disease progression and clinical outcome in patients at risk for coronary artery disease.6 Thus, the improvement of endothelial function by exercise is most likely to be of major importance for the atheroprotective effects of regular physical activity.
منابع مشابه
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...
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EXPRESSION OF INDUCIBLE NITRIC OXIDE SYNTHASE GENE (iNOS) STIMULATED BY HYDROGEN PEROXIDE IN HUMAN ENDOTHELIAL CELLS
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Cardiovascular disease is the single leading cause of death and morbidity for Canadians. A universal feature of cardiovascular disease is dysfunction of the vascular endothelium, thus disrupting control of vasodilation, tissue perfusion, hemostasis, and thrombosis. Nitric oxide bioavailability, crucial for maintaining vascular endothelial health and function, depends on the processes controllin...
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عنوان ژورنال:
- Circulation
دوره 107 25 شماره
صفحات -
تاریخ انتشار 2003