PMID- 17249527
OWN - NLM
STAT- MEDLINE
DCOM- 20070227
LR  - 20220227
IS  - 0916-9636 (Print)
IS  - 0916-9636 (Linking)
VI  - 29
IP  - 9
DP  - 2006 Sep
TI  - Pressure overload-induced transient oxidative stress mediates perivascular 
      inflammation and cardiac fibrosis through angiotensin II.
PG  - 711-8
AB  - Oxidative stress is implicated in the pathogenesis of various cardiovascular 
      diseases. We have shown that in Wistar rats with a suprarenal aortic constriction 
      (AC), pressure overload-induced transient perivascular inflammation (monocyte 
      chemoattractant protein-1 [MCP-1] induction and macrophage accumulation) in the 
      early phase is the determinant of reactive myocardial fibrosis and resultant 
      diastolic dysfunction in the late phase. Thus, we investigated the role of 
      reactive oxygen species production in cardiac remodeling in AC rats. Superoxide 
      production and the footprint of lipid peroxidation were assessed using 
      dihydroethidium staining and immunohistostaining against 4-hydroxy-2-nonenal 
      (4-HNE), respectively. In sham rats, dihydroethidium and 4-HNE signals were 
      scarcely found in the heart. At day 3, AC rats showed dihydroethidium signals 
      mainly in the intramyocardial arterial wall, whereas modest 4-HNE staining was 
      observed diffusely in the myocardium. These signals declined to lower levels by 
      day 14 despite sustained hypertension. Chronic administration of a subdepressor 
      dose of an angiotensin II type 1 receptor blocker candesartan reduced the 
      pressure overload-induced dihydroethidium and 4-HNE signals at day 3. Moreover, 
      candesartan decreased MCP-1 induction and macrophage infiltration at day 3 and 
      prevented myocardial fibrosis at day 14, without affecting left ventricle and 
      myocyte hypertrophy. In conclusion, acute pressure overload induced self-limited 
      superoxide production mainly in the vascular wall. The reactive oxygen species 
      production would contribute to the perivascular inflammation and subsequent 
      myocardial fibrosis. Angiotensin II was suggested to have a pressure-independent 
      effect on the reactive oxygen species production.
FAU - Kai, Hisashi
AU  - Kai H
AD  - Department of Internal Medicine Division of Cardio-Vascular Medicine, Kurume 
      University School of Medicine, Kurume, Japan. naikai@med.kurume0u.ac.jp
FAU - Mori, Takahiro
AU  - Mori T
FAU - Tokuda, Keisuke
AU  - Tokuda K
FAU - Takayama, Narimasa
AU  - Takayama N
FAU - Tahara, Nobuhiro
AU  - Tahara N
FAU - Takemiya, Kiyoko
AU  - Takemiya K
FAU - Kudo, Hiroshi
AU  - Kudo H
FAU - Sugi, Yusuke
AU  - Sugi Y
FAU - Fukui, Daisuke
AU  - Fukui D
FAU - Yasukawa, Hideo
AU  - Yasukawa H
FAU - Kuwahara, Fumitaka
AU  - Kuwahara F
FAU - Imaizumi, Tsutomu
AU  - Imaizumi T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Hypertens Res
JT  - Hypertension research : official journal of the Japanese Society of Hypertension
JID - 9307690
RN  - 0 (Angiotensin II Type 1 Receptor Blockers)
RN  - 0 (Benzimidazoles)
RN  - 0 (Biphenyl Compounds)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Tetrazoles)
RN  - 11128-99-7 (Angiotensin II)
RN  - S8Q36MD2XX (candesartan)
SB  - IM
CIN - Hypertens Res. 2006 Sep;29(9):643-4. PMID: 17249518
MH  - Angiotensin II/*physiology
MH  - Angiotensin II Type 1 Receptor Blockers/pharmacology
MH  - Animals
MH  - Benzimidazoles/pharmacology
MH  - Biphenyl Compounds
MH  - Fibrosis/pathology
MH  - Heart Ventricles/*metabolism/pathology
MH  - Hypertension/*physiopathology
MH  - Inflammation/physiopathology
MH  - Male
MH  - Oxidative Stress/drug effects/physiology
MH  - Rats
MH  - Rats, Wistar
MH  - Reactive Oxygen Species/*metabolism
MH  - Tetrazoles/pharmacology
MH  - Time Factors
MH  - Ventricular Remodeling/drug effects/*physiology
EDAT- 2007/01/26 09:00
MHDA- 2007/02/28 09:00
CRDT- 2007/01/26 09:00
PHST- 2007/01/26 09:00 [pubmed]
PHST- 2007/02/28 09:00 [medline]
PHST- 2007/01/26 09:00 [entrez]
AID - 10.1291/hypres.29.711 [doi]
PST - ppublish
SO  - Hypertens Res. 2006 Sep;29(9):711-8. doi: 10.1291/hypres.29.711.