Endothelial Dysfunction in Cardiovascular Diseases: The Role of Oxidant Stress
Hua Cai,David G. Harrison +1 more
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TL;DR: Accumulating evidence suggests that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone, and as the role of these various enzyme sources of ROS become clear, it will perhaps be possible to use more specific therapies to prevent their production and ultimately correct endothelial dysfunction.
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Abstract: Accumulating evidence suggests that oxidant stress alters many functions of the endothelium, including modulation of vasomotor tone. Inactivation of nitric oxide (NO(.)) by superoxide and other reactive oxygen species (ROS) seems to occur in conditions such as hypertension, hypercholesterolemia, diabetes, and cigarette smoking. Loss of NO(.) associated with these traditional risk factors may in part explain why they predispose to atherosclerosis. Among many enzymatic systems that are capable of producing ROS, xanthine oxidase, NADH/NADPH oxidase, and uncoupled endothelial nitric oxide synthase have been extensively studied in vascular cells. As the role of these various enzyme sources of ROS become clear, it will perhaps be possible to use more specific therapies to prevent their production and ultimately correct endothelial dysfunction.
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References
NAD(P)H Oxidase: Role in Cardiovascular Biology and Disease
TL;DR: Vascular NAD(P)H oxidases have been found to be essential in the physiological response of vascular cells, including growth, migration, and modification of the extracellular matrix and have been linked to hypertension and to pathological states associated with uncontrolled growth and inflammation, such as atherosclerosis.
3.1K
Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells.
TL;DR: The ability of Ang II to stimulate superoxide anion formation is examined and the identity of the oxidases responsible for its production is investigated to suggest that Ang II specifically activates enzyme systems that promote superoxide generation and raise the possibility that these pathways function as second messengers for long-term responses, such as hypertrophy or hyperplasia.
2.8K
Prognostic Impact of Coronary Vasodilator Dysfunction on Adverse Long-Term Outcome of Coronary Heart Disease
TL;DR: Coronary endothelial vasodilator dysfunction predicts long-term atherosclerotic disease progression and cardiovascular event rates and can provide pivotal information as both a diagnostic and prognostic tool in patients at risk for coronary heart disease.
2.8K
Angiotensin II-mediated hypertension in the rat increases vascular superoxide production via membrane NADH/NADPH oxidase activation. Contribution to alterations of vasomotor tone.
Sanjay Rajagopalan,S Kurz,Thomas Münzel,Margaret M. Tarpey,Bruce A. Freeman,Kathy K. Griendling,David G. Harrison +6 more
TL;DR: Forms of hypertension associated with elevated circulating levels of angiotensin II may have unique vascular effects not shared by other forms of hypertension because they increase vascular smooth muscle .O2- production via NADH/NADPH oxidase activation.
Hypercholesterolemia increases endothelial superoxide anion production.
TL;DR: Increased endothelial O2- production in HV may inactivate endothelium-derived nitric oxide and provide a source for other oxygen radicals, contributing to the early atherosclerotic process.