Nitric oxide and atherosclerosis

Claudio Napoli, Louis J. Ignarro

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)88-97
Number of pages10
JournalNitric Oxide - Biology and Chemistry
Issue number2
Publication statusPublished - 2001


  • Atherosclerosis
  • Coronary heart disease
  • Nitric oxide
  • Nitric oxide synthase
  • Page/paragraph/line

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology


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