Vascular Nitric Oxide and Oxidative Stress: Determinants of Endothelial Adaptations to Cardiovascular Disease and to Physical Activity

2005 ◽  
Vol 30 (4) ◽  
pp. 442-474 ◽  
Author(s):  
James W.E. Rush ◽  
Steven G. Denniss ◽  
Drew A. Graham

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 controlling synthesis and destruction of nitric oxide as well as on the sensitivity of target tissue to nitric oxide. Evidence supports a major contribution by oxidative stress-induced destruction of nitric oxide to the endothelial dysfunction that accompanies a number of cardiovascular disease states including hypertension, diabetes, chronic heart failure, and atherosclerosis. Regular physical activity (exercise training) reduces cardiovascular disease risk. Numerous studies support the hypothesis that exercise training improves vascular endothelial function, especially when it has been impaired by preexisting risk factors. Evidence is emerging to support a role for improved nitric oxide bioavailability with training as a result of enhanced synthesis and reduced oxidative stress-mediated destruction. Molecular targets sensitive to the exercise training effect include the endothelial nitric oxide synthase and the antioxidant enzyme superoxide dismutase. However, many fundamental details of the cellular and molecular mechanisms linking exercise to altered molecular and functional endothelial phenotypes have yet to be discovered. The working hypothesis is that some of the cellular mechanisms contributing to endothelial dysfunction in cardiovascular disease can be targeted and reversed by signals associated with regular increases in physical activity. The capacity for exercise training to regulate vascular endothelial function, nitric oxide bioavailability, and oxidative stress is an example of how lifestyle can complement medicine and pharmacology in the prevention and management of cardiovascular disease. Key words: exercise, artery, reactive oxygen species, antioxidant, hypertension

Aging ◽  
2017 ◽  
Vol 9 (1) ◽  
pp. 187-208 ◽  
Author(s):  
Jessica R. Santos-Parker ◽  
Talia R. Strahler ◽  
Candace J. Bassett ◽  
Nina Z. Bispham ◽  
Michel B. Chonchol ◽  
...  

2015 ◽  
Vol 34 (4) ◽  
pp. 300-307 ◽  
Author(s):  
Swati Omanwar ◽  
M. Fahim

Vascular endothelium plays a vital role in the organization and function of the blood vessel and maintains homeostasis of the circulatory system and normal arterial function. Functional disruption of the endothelium is recognized as the beginning event that triggers the development of consequent cardiovascular disease (CVD) including atherosclerosis and coronary heart disease. There is a growing data associating mercury exposure with endothelial dysfunction and higher risk of CVD. This review explores and evaluates the impact of mercury exposure on CVD and endothelial function, highlighting the interplay of nitric oxide and oxidative stress.


2014 ◽  
Vol 20 (1) ◽  
pp. 135-145 ◽  
Author(s):  
Stephanie Lankhorst ◽  
Mariëtte H.W. Kappers ◽  
Joep H.M. van Esch ◽  
A.H. Jan Danser ◽  
Anton H. van den Meiracker

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