The vascular biology of nitric oxide and its role in atherogenesis.
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.
Lloyd-Jones
D M
DM
Cardiac Unit, Massachusetts General Hospital, Harvard Medical School, Boston 02114, USA.
Bloch
K D
KD
D000800:Angioplasty, Balloon; D000818:Animals; D001161:Arteriosclerosis / Q000503:physiopathology*; D006152:Cyclic GMP / Q000502:physiology; D004730:Endothelium, Vascular / Q000293:injuries / Q000503:physiopathology*; D005352:Fibromuscular Dysplasia / Q000503:physiopathology; D006801:Humans; D009569:Nitric Oxide / Q000502:physiology*; D012008:Recurrence; D015398:Signal Transduction / Q000502:physiology
D009569:Nitric Oxide; D006152:Cyclic GMP