PMID- 10645927
OWN - NLM
STAT- MEDLINE
DCOM- 20000210
LR  - 20190623
IS  - 1524-4539 (Electronic)
IS  - 0009-7322 (Linking)
VI  - 101
IP  - 3
DP  - 2000 Jan 25
TI  - 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.
PG  - 305-10
AB  - 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-kappaB 
      (NF-kappaB, 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.
FAU - Usui, M
AU  - Usui M
AD  - Research Institute of Angiocardiology, Kyushu University Faculty of Medicine, 
      Fukuoka, Japan.
FAU - Egashira, K
AU  - Egashira K
FAU - Tomita, H
AU  - Tomita H
FAU - Koyanagi, M
AU  - Koyanagi M
FAU - Katoh, M
AU  - Katoh M
FAU - Shimokawa, H
AU  - Shimokawa H
FAU - Takeya, M
AU  - Takeya M
FAU - Yoshimura, T
AU  - Yoshimura T
FAU - Matsushima, K
AU  - Matsushima K
FAU - Takeshita, A
AU  - Takeshita A
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Circulation
JT  - Circulation
JID - 0147763
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor, Angiotensin, Type 1)
RN  - 0 (Receptor, Angiotensin, Type 2)
RN  - 0 (Receptors, Angiotensin)
RN  - 11062-77-4 (Superoxides)
RN  - 11128-99-7 (Angiotensin II)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - EC 3.4.15.1 (Peptidyl-Dipeptidase A)
RN  - V55S2QJN2X (NG-Nitroarginine Methyl Ester)
SB  - IM
MH  - Angiotensin II/*physiology
MH  - Animals
MH  - Chemokine CCL2/analysis/genetics
MH  - Coronary Vessels/*pathology
MH  - Inflammation/*etiology
MH  - Male
MH  - NF-kappa B/metabolism
MH  - NG-Nitroarginine Methyl Ester/*toxicity
MH  - Nitric Oxide/*physiology
MH  - Peptidyl-Dipeptidase A/metabolism
MH  - RNA, Messenger/analysis
MH  - Rats
MH  - Rats, Inbred WKY
MH  - Receptor, Angiotensin, Type 1
MH  - Receptor, Angiotensin, Type 2
MH  - Receptors, Angiotensin/*physiology
MH  - Superoxides/metabolism
EDAT- 2000/01/25 00:00
MHDA- 2000/01/25 00:01
CRDT- 2000/01/25 00:00
PHST- 2000/01/25 00:00 [pubmed]
PHST- 2000/01/25 00:01 [medline]
PHST- 2000/01/25 00:00 [entrez]
AID - 10.1161/01.cir.101.3.305 [doi]
PST - ppublish
SO  - Circulation. 2000 Jan 25;101(3):305-10. doi: 10.1161/01.cir.101.3.305.