Abstract
The in vitro observations of Furchgott and Zawadzki [1] and the in vitro and in vivo reports from the group of Moncada [2, 3] have shown that an endothelium-derived-relaxing-factor, identified as nitric oxide [2], modulates vascular tone in response to physiologic and pathologic stimuli (increase in wall shear stress, serotonin, bradykinin, histamine, thrombin, sympathetic stimulation, acetylcholine, endotoxins, etc.). Endothelial damage, leading to a decreased formation or release of nitric oxide from its precursor L-arginine, or reduced penetration due to the presence of subendothelial intimal thickening, are possible explanations of the impairment of endothelium-mediated vasodilatation observed in patients with systemic hypertension [4], hypercholesterolemia, diabetes mellitus [5], atherosclerosis [6].
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Mario, C.D., Strikwerda, S., Gil, R., De Feyter, P.J., Meneveau, N., Serruys, P.W. (1994). Response of conductance and resistance coronary vessels to scalar concentrations of acetylcholine. Assessment with quantitative angiography and intracoronary Doppler in 29 patients with coronary artery disease. In: Serruys, P.W., Foley, D.P., De Feyter, P.J. (eds) Quantitative Coronary Angiography in Clinical Practice. Developments in Cardiovascular Medicine, vol 145. Springer, Dordrecht. https://doi.org/10.1007/978-94-015-8358-9_19
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DOI: https://doi.org/10.1007/978-94-015-8358-9_19
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