1996
DOI: 10.1016/0735-1097(95)00521-8 View full text |Buy / Rent full text
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Abstract: We conclude that nitric oxide normally exerts a substantial tonic dilating effect in coronary collateral vessels. Disease-induced alterations in endothelial function may limit collateral perfusion importantly.

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“…[36][37][38] Nitric oxide (NO), an endothelial-derived relaxing factor with antiatherogenic properties, counters ET-1 contributing to coronary artery dilation. [39] Although NO maintains adequate blood flow through coronary collaterals of CAD patients, [40] normal NO production elicited by endothelium-dependent stimuli in healthy coronary arteries, is found to be markedly impaired in diseased arteries, whereas ET-1 levels are increased. [38,41,42] Vascular inflammation contributes to atherosclerosis and recurrent ischemic cardiac outcomes.…”
Section: The Ras Genetic Contribution To Cadmentioning
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“…[36][37][38] Nitric oxide (NO), an endothelial-derived relaxing factor with antiatherogenic properties, counters ET-1 contributing to coronary artery dilation. [39] Although NO maintains adequate blood flow through coronary collaterals of CAD patients, [40] normal NO production elicited by endothelium-dependent stimuli in healthy coronary arteries, is found to be markedly impaired in diseased arteries, whereas ET-1 levels are increased. [38,41,42] Vascular inflammation contributes to atherosclerosis and recurrent ischemic cardiac outcomes.…”
Section: The Ras Genetic Contribution To Cadmentioning
“…Increased vascular RAS activity in the setting of certain RAS polymorphisms would likely affect major contributing components of CAD risk; these include fibrinolytic balance, vascular endothelial function, vascular inflammation, and vascular proliferation-among others. [34][35][36][37][38][39][40][41][42][43][44][45][46][47][48][49] Notable pathophysiologic mechanisms are discussed in general terms below.…”
Section: The Ras Genetic Contribution To Cadmentioning
“…There is evidence that endogenous NO preferentially influences the tone of the conduit vessels with a declining gradient along the coronary vascular bed towards the periphery, while exogenously administered NO leads to uniform dilatation throughout the coronary vascular bed [12][13][14]. Further, NO also has a tonic influence on the diameter of collateral vessels [15]. Constitutive expression of the endothelial NO synthase takes place mainly in the conduit vessels and large resistance arteries, with decreasing intensity toward the capillaries [16][17][18].…”
Section: Introductionmentioning
“…Many vascular insults impair endothelial function. Endothelial dysfunction causes heterogeneous, altered vasomotor tone at resting conditions due to altered nitric oxide production with increased vasoconstriction at rest as well as vasoconstrictive responses to a variety of stimuli that normally cause vasodilation, such as acetylcholine and exercise [3][4][5][6][7][8][9][10][11][12][13][14][15][16][17].…”
Section: Introductionmentioning