Chronic inhibition of nitric oxide synthesis in rats increases aortic superoxide anion production via the action of angiotensin II
作者:
Shiro Kitamoto,
Kensuke Egashira,
Chu Kataoka,
Makoto Usui,
Masamichi Koyanagi,
Masao Takemoto,
Akira Takeshita,
期刊:
Journal of Hypertension
(OVID Available online 2000)
卷期:
Volume 18,
issue 12
页码: 1795-1800
ISSN:0263-6352
年代: 2000
出版商: OVID
关键词: nitric oxide;angiotensin;arteriosclerosis;endothelium-derived factors;remodeling
数据来源: OVID
摘要:
ObjectiveChronic inhibition of nitric oxide (NO) synthesis by Nω-nitro-L-arginine methyl ester (L-NAME) increases vascular tissue angiotensin II activity and oxidative stress in animals by incompletely understood mechanisms. In a rat model, we investigated the role of local angiotensin II activity in the pathogenesis of increased oxidative stress.DesignWe studied the aortas of control rats and others receiving L-NAME or L-NAME plus an angiotensin II type 1 receptor antagonist (CS-866).ResultsAdministration of L-NAME for 7 days significantly increased superoxide anion (O2−) and both immunoreactivity and electrophoretically demonstrable activity of redox-sensitive transcription factors (NF-κB and AP-1). Treatment with the angiotensin II type 1 receptor antagonist prevented all of the above changes. The observed effects of the type 1 receptor antagonist was independent of the L-NAME-induced arterial hypertension.ConclusionsThese findings suggest that chronic inhibition of NO synthesis may increase vascular oxidative stress and oxidative stress-sensitive signals via the action of angiotensin II mediated via type 1 receptors.
点击下载:
PDF
(255KB)
返 回