Nitric oxide, nitric oxide synthase, and hypertensive vascular disease

被引：18

作者：

Busse R. ^{[1
]}

Fleming I. ^{[1
]}

机构：

[1] Institut Für Kardiovaskuläre Physiologie, Klinikum der J. W. Goethe-Universität, Theodor-Stern-Kai 7

来源：

Current Hypertension Reports | 1999年 / 1卷 / 1期

关键词：

Nitric Oxide; Essential Hypertension; Fluid Shear Stress; eNOS Expression; eNOS Gene;

D O I：

10.1007/s11906-999-0078-6

中图分类号：

学科分类号：

摘要：

In normotension the endothelium produces mainly nitric oxide (NO) and prostacyclin, and the vasodilator and growth inhibitory influence predominates. Hypertension, however, is associated with a shift towards enhanced constriction and vascular hypertrophy. These effects are associated with an apparent decrease in the production of bioactive NO and concomitant increase in the generation of oxygen-derived free radicals, such as superoxide anions (O2-). While the enzymatic source of endothelial O2- has been debated intensely over the past few years, it may well turn out that the endothelial NO synthase is itself an important producer of O2-. Because the redox state of endothelial cells and, for example, the activation of redoxsensitive transcription factors is regulated by the balance between NO and O2- production, endothelial NO synthase may well be the most crucial enzyme determining the antior prohypertensive and eventually proatherogenic state of the vascular wall. Copyright © 1999 by Current Science Inc.

引用

页码：88 / 95

页数：7

共 87 条

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