NAD(P)H oxidase inhibitor prevents blood pressure elevation and cardiovascular hypertrophy in aldosterone-infused rats

被引:112
作者
Park, YM
Park, MY
Suh, YL
Park, JB [1 ]
机构
[1] Sungkyunkwan Univ, Sch Med, Samsung Cheil Hosp, Dept Med Cardiol, Seoul, South Korea
[2] Samsung Biomed Res Inst, Seoul, South Korea
[3] Sungkyunkwan Univ, Sch Med, Samsung Med Ctr, Dept Pathol, Seoul, South Korea
关键词
fibrosis; hypertension; aldosterone-infused rats; NAD(P)H oxidase;
D O I
10.1016/j.bbrc.2003.11.173
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Increased bioavailability of reactive oxygen species (ROS) has been implicated in the pathogenesis of mineralocorticoid hypertension. To find out the source of ROS, we evaluated the role of NAD(P)H oxidase in blood pressure (BP) elevation, cardiovascular hypertrophy, and fibrosis in aldosterone-salt rats. Aldosterone infusion (0.75 mug/h) significantly increased BP, which is attenuated by apocynin (1.5 mmol/L). Cardiac hypertrophy developed by aldosterone infusion was also normalized with apocynin. Greater mRNA for p22phox and NAD(P)H oxidase activity (more than twofold) in aorta of aldosterone-infused rats was reduced in apocynin-treated rats. Aldosterone infusion increased marginally procollagen I and III expression in LV compared to controls and apocynin decreased procollagen. Masson's Trichrome stain showed increased cardiac perivascular fibrosis, which was reduced by apocynin. These results suggest that NAD(P)H oxidase plays an important role in cardiovascular damage associated with mineralocorticoid hypertension. (C) 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:812 / 817
页数:6
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