Chronic inhibition of nitric oxide synthesis in rats increases aortic superoxide anion production via the action of angiotensin II

Shiro Kitamoto, Kensuke Egashira, Chu Kataoka, Makoto Usui, Masamichi Koyanagi, Masao Takemoto, Akira Takeshita

Research output: Contribution to journalArticle

60 Citations (Scopus)

Abstract

Objective: Chronic inhibition of nitric oxide (NO) synthesis by N(w)-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. Design: We studied the aortas of control rats and others receiving L-NAME or L-NAME plus an angiotensin II type 1 receptor antagonist (CS-866). Results: Administration 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. Conclusions: These 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. (C) 2000 Lippincott Williams and Wilkins.

Original languageEnglish
Pages (from-to)1795-1800
Number of pages6
JournalJournal of hypertension
Volume18
Issue number12
DOIs
Publication statusPublished - 2000

All Science Journal Classification (ASJC) codes

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine

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