Mineralocorticoid receptor antagonist eplerenone alleviates the reduction and dysfunction of endothelial progenitor cells in hypertensive patients

被引:0
作者
Wang, Huanhuan [1 ]
Zhu, Aoshuang [1 ]
Wang, Xin [1 ]
Zang, Xuan [1 ]
Huang, Changgen [1 ]
Zhao, Jianzhong [1 ]
Ding, Zhijian [1 ]
机构
[1] Southeast Univ, Dept Cardiol, Affiliated Zhongda Hosp, 87 Dingjiaqiao, Nanjing 02013, Jiangsu, Peoples R China
关键词
Hypertension; aldosterone; endothelial progenitor cells; cell migration; leukocyte adhesion; NITRIC-OXIDE SYNTHASE; CORONARY-ARTERY-DISEASE; CARDIOVASCULAR RISK; REPAIR CAPACITY; ALDOSTERONE; MOBILIZATION; SYSTEM; REENDOTHELIALIZATION; HYPERALDOSTERONISM; FIBROBLASTS;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The aim of this study was to investigate the effects of antagonist of aldosterone/mineralocorticoid receptor (MR) on the amount, adhesion and migration capacity of EPCs of hypertensive patients. Human EPCs were isolated from peripheral blood by Ficoll density-gradient centrifugation and confirmed by uptake of acetylated LDL and binding of ulex-lectin. Adhesion assays and migration assays were used to determine the function of EPCs. The expression levels of MR, eNOS, and CYP11B2 were assessed by qRT-PCR and Western-blot. The serum SDF-1 level was determined by EUSA assay. Serum SDF-1 level was elevated in hypertensive patients and was suppressed by eplerenone. The migration and adhesion abilities of EPCs were reduced in patients but the reduction was partially reversed by eplerenone. The expression levels of MR and CYP11B2 were significantly increased but that of eNOS was markedly decreased in patients with hypertension, and the changes were suppressed after aldosterone/MR antagonist Eplerenone treatment. The present study indicated that elevated aldosterone level caused reduction and dysfunction of endothelial progenitor cells in hypertensive patients, aldosterone/MR antagonist Eplerenone can partially reverse effects caused by the increase of aldosterone.
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收藏
页码:7979 / 7986
页数:8
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