Inducible nitric oxide synthase and vascular injury

被引：128

作者：

Kibbe, M ^{[1
]}

Billiar, T ^{[1
]}

Tzeng, E ^{[1
]}

机构：

[1] Univ Pittsburgh, Dept Surg, Pittsburgh, PA 15261 USA

来源：

CARDIOVASCULAR RESEARCH | 1999年 / 43卷 / 03期

关键词：

nitric oxide; inducible nitric oxide synthase; vasoprotection; vascular injury;

D O I：

10.1016/S0008-6363(99)00130-3

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

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. (C) 1999 Elsevier Science B.V. All rights reserved.

引用

页码：650 / 657

页数：8