The vascular biology of nitric oxide and its role in atherogenesis

Donald M. Lloyd-Jones*, Kenneth D. Bloch

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

200 Scopus citations

Abstract

Nitric oxide (NO), the biologically active component of endothelium-derived relaxing factor, has critical roles in the maintenance of vascular homeostasis. Decreased endothelial NO production, as a result of endothelial dysfunction, occurs in the early phases of atherosclerosis. NO appears to inhibit atherogenesis by inhibiting leukocyte and platelet activation and by inhibiting smooth muscle cell proliferation. Endothelial denudation is a prominent feature of vascular injury associated with percutaneous angioplasty, and decreased NO production appears to contribute to the restenosis process. Manipulation of the NO/cGMP signal transduction system may provide novel therapeutic approaches for limiting atherogenesis and neointimal proliferation in the future.

Original languageEnglish (US)
Pages (from-to)365-375
Number of pages11
JournalAnnual review of medicine
Volume47
DOIs
StatePublished - May 20 1996

Keywords

  • Endothelium
  • Endothelium-derived relaxing factor
  • Neointimal formation
  • Restenosis
  • Signal transduction

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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