Physical Inactivity Increases Oxidative Stress, Endothelial Dysfunction, and Atherosclerosis

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Physical inactivity increases oxidative stress, endothelial dysfunction, and atherosclerosis.

OBJECTIVE Sedentary lifestyle is associated with increased cardiovascular events. The underlying molecular mechanisms are incompletely understood. Reactive oxygen species (ROS) contribute to endothelial dysfunction and atherosclerosis. An important source of vascular ROS is the NADPH oxidase. METHODS AND RESULTS C57BL6 mice were subjected to regular housing (physical inactivity) or voluntary ...

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Enforced physical inactivity increases endothelial microparticle levels in healthy volunteers.

A sedentary lifestyle has adverse effects on the cardiovascular system, including impaired endothelial functions. Subjecting healthy men to 7 days of dry immersion (DI) presented a unique opportunity to analyze the specific effects of enhanced inactivity on the endothelium. We investigated endothelial properties before, during, and after 7 days of DI involving eight subjects. Microcirculatory f...

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Physical inactivity causes endothelial dysfunction in healthy young mice.

OBJECTIVES We sought to determine if physical inactivity affects endothelial function in young healthy individuals. BACKGROUND Recent studies have linked exercise training to increased bioavailability of vascular nitric oxide (NO) and to improved endothelial function in patients with cardiovascular disorders. The effects of physical inactivity on normal vascular endothelial function are not k...

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Oxidative stress and endothelial dysfunction during sepsis.

Endothelial activation and dysfunction play a key role in the pathogenesis of sepsis. During septic shock, endothelial dysfunction is involved in microcirculation impairment and organ dysfunction. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) have several potentially important effects on endothelial function and are implicated in physiological regulation and disease pathophy...

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[Endothelial dysfunction and atherosclerosis].

Mammalian endothelium acts as a mediator in arterial and venous relaxation and contraction. Endothelium-dependent relaxation is due to endothelial release of powerful, non-prostanoid vasodilatory substances. The best known of these is the endothelial factor EDRF identified as nitrous oxide (NO). It is the end result of the metabolism of L-arginine by the NO synthetase of endothelial cells. In a...

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ژورنال

عنوان ژورنال: Arteriosclerosis, Thrombosis, and Vascular Biology

سال: 2005

ISSN: 1079-5642,1524-4636

DOI: 10.1161/01.atv.0000158311.24443.af