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Inducible nitric oxide synthase and vascular injury

Authors :
Edith Tzeng
Timothy R. Billiar
Melina R. Kibbe
Source :
Cardiovascular Research. 43:650-657
Publication Year :
1999
Publisher :
Oxford University Press (OUP), 1999.

Abstract

The role nitric oxide (NO) plays in the cardiovascular system is complex and diverse. Even more controversial is the role that the inducible NO synthase enzyme (iNOS) serves in mediating different aspects of cardiovascular pathophysiology. Following arterial injury, NO has been shown to serve many vasoprotective roles, including inhibition of platelet aggregation and adherence to the site of injury, inhibition of leukocyte adherence, inhibition of vascular smooth muscle cell (VSMC) proliferation and migration, and stimulation of endothelial cell (EC) growth. These properties function together to preserve a normal vascular environment following injury. In this review, we discuss what is known about the involvement of iNOS in the vascular injury response. Additionally, we discuss the beneficial role of iNOS gene transfer to the vasculature in preventing the development of neointimal thickening. Lastly, the pathophysiology of transplant vasculopathy is discussed as well as the role of iNOS in this setting.

Details

ISSN :
00086363
Volume :
43
Database :
OpenAIRE
Journal :
Cardiovascular Research
Accession number :
edsair.doi.dedup.....b8a4a949a85dc21d3d02f0da153d0d96
Full Text :
https://doi.org/10.1016/s0008-6363(99)00130-3