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Important role of local angiotensin II activity mediated via type 1 receptor in the pathogenesis of cardiovascular inflammatory changes induced by chronic blockade of nitric oxide synthesis in rats

  1. Author:
    Usui, M.
    Egashira, K.
    Tomita, H.
    Koyanagi, M.
    Katoh, M.
    Shimokawa, H.
    Takeya, M.
    Yoshimura, T.
    Matsushima, K.
    Takeshita, A.

  2. Author Address

    Egashira K Kyushu Univ, Sch Med, Angiocardiol Res Inst, Higashi Ku 3-1-1 Maidashi Fukuoka 8128582 Japan Kyushu Univ, Sch Med, Angiocardiol Res Inst, Higashi Ku Fukuoka 8128582 Japan Kumamoto Univ, Sch Med, Dept Pathol 2 Kumamoto 860 Japan Univ Tokyo, Sch Med, Dept Mol Prevent Med Tokyo 113 Japan NCI, Immunopathol Sect, Immunobiol Lab Frederick, MD 21701 USA
    1. Year: 2000
  2. Journal: Circulation
    1. 101
    2. 3
    3. Pages: 305-310
  4. Type of Article: Article
  1. Abstract:

    Background-The chronic inhibition of NO synthesis by N-omega-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-kappa B (NF-kappa B, 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. [References: 38]

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