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Angiotensin II‐Induced Cardiac Vascular Remodeling: Role of Oxidative Stress
Author(s) -
Zhao Wenyuan,
Zhao Dan,
Chen Yuanjian,
Jiang youde,
Sun Yao
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1144-d
Subject(s) - angiotensin ii , apocynin , oxidative stress , medicine , nadph oxidase , endocrinology , cardiac fibrosis , reactive oxygen species , fibrosis , malondialdehyde , superoxide dismutase , vascular smooth muscle , ventricular remodeling , heart failure , chemistry , blood pressure , biochemistry , smooth muscle
Cardiac vascular remodeling occurs in patients with hypertension and chronic heart failure, which is related to elevated circulating angiotensin (Ang)II. The underlying mechanisms involved in AngII‐induced cardiac remodeling are not completely defined. AngII stimulates reactive oxygen species (ROS) production by activating NHDPH oxidase. Herein, we detected whether oxidative stress contributes to AngII‐induced cardiac vascular remodeling. SD rats (n=8/group) were treated with AngII (150ug/min) for 4 wks. NADPH oxidase inhibitor apocynin (120mg/kg/day) together with a superoxide dismutase mimetic, tempol (120mg/kg/day) were given in combination with AngII infusion. Untreated rats served as controls. Compared to controls, in rats with AngII treatment we found significantly increased cardiac levels of malondialdehyde (MDA, a product of lipid oxidation), accumulated ED‐1+ macrophages and ‐smooth muscle actin+ myofibroblasts in the perivascular space of coronary arteries, significantly increased TGF‐ 1 mRNA, and appearance of fibrosis in the perivascular space. Combined antioxidant treatment suppressed cardiac MDA levels, significantly reduced expression of TGF‐ 1 in perivascular space and decreased perivascular fibrosis. Thus, the current study suggests that oxidative stress partially mediate AngII‐induced cardiac vascular repair/remodeling.