(Circulation. 2000;101:305.)
© 2000 American Heart Association, Inc.
Basic Science Reports |
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
From the Research Institute of Angiocardiology, Kyushu University Faculty of Medicine, Fukuoka (M.U., K.E., H.T., M. Koyanagi, M. Katoh, H.S., A.T.); the Second Department of Pathology, Kumamoto University School of Medicine, Kumamoto (M.T.); and the Department of Molecular Preventive Medicine, University of Tokyo School of Medicine, Tokyo (K.M.), Japan; and the Immunopathology Section, Laboratory of Immunobiology, National Cancer Institute, Frederick, Md (T.Y.).
Correspondence to Kensuke Egashira, MD, PhD, Research Institute of Angiocardiology and Cardiovascular Clinic, Kyushu University School of Medicine, 3-1-1, Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. e-mail egashira{at}cardiol.med.kyushu-u.ac.jp
Background—The chronic inhibition
of NO synthesis by
N
-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-
B (NF-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.
Key Words: endothelium-derived factors • nitric oxide • remodeling • proteins • cells
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