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Cardiovascular Research 1999 43(3):650-657; doi:10.1016/S0008-6363(99)00130-3
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

Inducible nitric oxide synthase and vascular injury

Melina Kibbe*, Timothy Billiar and Edith Tzeng

University of Pittsburgh, Department of Surgery, 677 Scaife Hall, Pittsburgh, PA 15261, USA

* Corresponding author. Tel.: +1-412-648-1935; fax: +1-412-624-1172 kibbemr{at}msx.upmc.edu

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.

KEYWORDS Nitric oxide; Inducible nitric oxide synthase; Vasoprotection; Vascular injury


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