Pressure Overload–Induced Transient Oxidative Stress Mediates Perivascular Inflammation and Cardiac Fibrosis through Angiotensin II

被引:0
作者
Hisashi Kai
Takahiro Mori
Keisuke Tokuda
Narimasa Takayama
Nobuhiro Tahara
Kiyoko Takemiya
Hiroshi Kudo
Yusuke Sugi
Daisuke Fukui
Hideo Yasukawa
Fumitaka Kuwahara
Tsutomu Imaizumi
机构
[1] Kurume University School of Medicine,Department of Internal Medicine Division of Cardio
[2] Cardiovascular Research Institute,Vascular Medicine
[3] Kurume University,undefined
来源
Hypertension Research | 2006年 / 29卷
关键词
oxidative stress; hypertension; macrophage; fibrosis;
D O I
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中图分类号
学科分类号
摘要
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.
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页码:711 / 718
页数:7
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