期刊
NITRIC OXIDE-BIOLOGY AND CHEMISTRY
卷 5, 期 2, 页码 88-97出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/niox.2001.0337
关键词
nitric oxide; nitric oxide synthase; atherosclerosis; coronary heart disease; page/paragraph/line
Endothelial dysfunction has been shown in a wide range of vascular desorders including atherosclerosis and related diseases. Here, we examine and address the complex relationship among nitric oxide (NO)-mediated pathways and atherogenesis. In view of the numerous pathophysiological actions of NO, abnormalities could potentially occur at many sites: (a) impairment of membrane receptors in the arterial wall that interact with agonists or physiological stimuli capable of generating NO; (b) reduced concentrations or impaired utilization of L-arginine; (c) reduction in concentration or activity both of inducible and endothelial NO synthase; (d) impaired release of NO from the atherosclerotic damaged endothelium; (e) impaired NO diffusion from endothelium to vascular smooth muscle cells followed by decreased sensitivity to its vasodilator action; (f) local enhanced degradation of NO by increased generation of free radicals and/or oxidation-sensitive mechanisms; and (g) impaired interaction of NO with guanylate cyclase and consequent limitation of cyclic GMP production. Therefore, one target for new drugs should be the preservation or restoration of NO-mediated signaling pathways in arteries. Such novel therapeutic strategies may include administration of L-arginine/antioxidants and gene-transfer approaches, (C) 2001 Academic Press.
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