Important role of local angiotensin II activity mediated via type I receptor in the pathogenesis of cardiovascular inflammatory changes induced by chronic blockade of nitric oxide synthesis in rats

Makoto Usui, Kensuke Egashira, Hideharu Tomita, Masamichi Koyanagi, Makoto Katoh, Hiroaki Shimokawa, Motohiro Takeya, Teizo Yoshimura, Kouji Matsushima, Akira Takeshita

研究成果: Contribution to journalArticle査読

159 被引用数 (Scopus)

抄録

Background - The chronic inhibition of NO synthesis by N(ω)-nitro-L- arginine methyl ester (L-NAME) upregulates the cardiovascular tissue angiotensin II (Ang II)-generating system and induces cardiovascular inflammatory changes in rats. Methods and Results - We used a rat model to investigate the role of local Ang II activity in the pathogenesis of such inflammatory changes. Marked increases in monocyte infiltration into coronary vessels and myocardial interstitial areas, monocyte chemoattractant protein-1 (MCP-1) expression, and nuclear factor-κB (NF-κB, an important redox- sensitive transcriptional factor that induces MCP-1) activity were observed on day 3 of L-NAME administration. Along with these changes, vascular superoxide anion production was also increased. Treatment with an Ang II type 1 receptor antagonist or with a thiol-containing antioxidant, N- acetylcysteine, prevented all of these changes. Conclusions - Increased Ang II activity mediated via the type 1 receptor may thus be important in the pathogenesis of early cardiovascular inflammatory changes in this model. Endothelium-derived NO may decrease MCP-1 production and oxidative stress- sensitive signals by suppressing localized activity of Ang II.

本文言語英語
ページ(範囲)305-310
ページ数6
ジャーナルCirculation
101
3
DOI
出版ステータス出版済み - 1 25 2000

All Science Journal Classification (ASJC) codes

  • 循環器および心血管医学
  • 生理学(医学)

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