Pathogenic Role of Oxidative Stress in Vascular Angiotensin-Converting Enzyme Activation in Long-Term Blockade of Nitric Oxide Synthesis in Rats
作者:
Makoto Usui,
Kensuke Egashira,
Shiro Kitamoto,
Masamichi Koyanagi,
Makoto Katoh,
Chu Kataoka,
Hiroaki Shimokawa,
Akira Takeshita,
期刊:
Hypertension
(OVID Available online 1999)
卷期:
Volume 34,
issue 4, Part 1
页码: 546-551
ISSN:0194-911X
年代: 1999
出版商: OVID
关键词: nitric oxide;stress, oxidative;anions;angiotensin-converting enzyme;remodeling
数据来源: OVID
摘要:
Inhibition of nitric oxide (NO) synthesis withNω-nitro-L-arginine methyl ester (L-NAME) activates vascular angiotensin-converting enzyme (ACE) and causes oxidative stress. We investigated the role of oxidative stress in the pathogenesis of ACE activation in rats. Studies involved aortas of rats receiving no treatment, L-NAME, L-NAME plus L-arginine, or L-NAME plus an antioxidant drug (N-acetylcysteine, allopurinol, or ebselen) for 7 days. L-NAME significantly increased oxidative stress (O2−) and ACE activity. The increased O2−production was normalized by removal of endothelium. Immunohistochemistry showed the increased ACE activity in the endothelial layer. Treatment with antioxidant drugs did not affect the L-NAME-induced increase in systolic arterial pressure but did prevent increases in vascular O2−production and ACE activity. These results implicate oxidative stress in the pathogenesis of vascular ACE activation in rats with long-term inhibition of NO synthesis. The observed effects of antioxidant drugs on ACE activation do not appear to involve the hypertension induced by L-NAME.
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