IR@PKUHSC  > 北京大学基础医学院  > 心血管所
学科主题基础医学
Endogenous aldosterone is involved in vascular calcification in rat
Wu, Sheng-Ying1,2; Yu, Yan-Rong1,3; Cai, Yan1,2; Jia, Li-Xin4; Wang, Xiong2; Xiao, Chuan-Shi4; Tang, Chao-Shu1,2; Qi, Yong-Fen1
关键词Aldosterone Blood Vessel Calcification Fibrosis Rat
刊名EXPERIMENTAL BIOLOGY AND MEDICINE
2012
DOI10.1258/ebm.2011.011175
237期:1页:31-37
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Medicine, Research & Experimental
研究领域[WOS]Research & Experimental Medicine
关键词[WOS]SMOOTH-MUSCLE-CELLS ; ANGIOTENSIN-II ; MINERALOCORTICOID RECEPTOR ; CARDIOVASCULAR-SYSTEM ; OXIDATIVE STRESS ; MECHANISMS ; ADRENOMEDULLIN ; CALCIUM ; PATHWAY ; TARGET
英文摘要

Aldosterone (Aldo) is an important active hormone in the renin-angiotensin-aldosterone system and plays a vital role in the development of hypertension, heart failure and other cardiovascular diseases. We aimed to explore the role of endogenous Aldo in aortic calcification in rats. We induced arterial calcification in rats by intramuscular administration of vitamin D-3 plus oral nicotine (VDN) and determined calcium content, Ca-45(2+) accumulation and activity of alkaline phosphatase (ALP). The mRNA level of osteopontin (OPN) was measured by semi-quantitative reverse transcriptase polymerase chain reaction. Deposition of collagen in the aorta wall was measured by Sirius red staining. The content of angiotensin II (Ang II) and Aldo in plasma and myocardial and vascular tissue was determined by radioimmunoassay. In rats with VDN treatment, von Kossa staining showed calcification in vascular smooth muscle cells and extracellular matrix, and the content of calcium in calcified arteries was 5.8-fold of that in control arteries (P < 0.01). The accumulation of Ca-45(2+) and activity of ALP in calcified aortic tissue was three- and 2.5-fold, respectively, that in control tissue (P < 0.01). The mRNA expression of OPN was significantly higher, by 58%, in calcified than control tissue (P < 0.01). Vascular fibrosis was greater in rats with calcified tissue than in control rats. The level of Ang II and Aldo was 58% and 80% higher, respectively, in calcified than control tissue (both P < 0.01). The changes could be significantly improved by treatment with captopril, an angiotensin-converting enzyme inhibitor, and the Aldo receptor antagonist spironolactone. These results suggest that Aldo is an endogenous bioactive factor involved in vascular calcification.

语种英语
WOS记录号WOS:000299865600005
项目编号30770869 ; 30871013 ; 81070090
资助机构National Natural Science Foundation of China ; Beijing Municipal Commission of Education
引用统计
被引频次:26[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/52593
专题北京大学基础医学院_心血管所
北京大学基础医学院
作者单位1.Peking Univ, Hlth Sci Ctr, Key Lab Mol Cardiovasc Sci, Minist Educ, Beijing 100191, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Dept Med Parasitol, Sch Basic Med Sci, Beijing 100191, Peoples R China
4.Shanxi Med Univ, Dept Cardiol, Hosp 2, Taiyuan 030001, Shanxi, Peoples R China
推荐引用方式
GB/T 7714
Wu, Sheng-Ying,Yu, Yan-Rong,Cai, Yan,et al. Endogenous aldosterone is involved in vascular calcification in rat[J]. EXPERIMENTAL BIOLOGY AND MEDICINE,2012,237(1):31-37.
APA Wu, Sheng-Ying.,Yu, Yan-Rong.,Cai, Yan.,Jia, Li-Xin.,Wang, Xiong.,...&Qi, Yong-Fen.(2012).Endogenous aldosterone is involved in vascular calcification in rat.EXPERIMENTAL BIOLOGY AND MEDICINE,237(1),31-37.
MLA Wu, Sheng-Ying,et al."Endogenous aldosterone is involved in vascular calcification in rat".EXPERIMENTAL BIOLOGY AND MEDICINE 237.1(2012):31-37.
条目包含的文件
文件名称/大小 文献类型 版本类型 开放类型 使用许可
ebm%2E2011%2E011175.(354KB)期刊论文作者接受稿开放获取CC BY-NC-SA浏览 请求全文
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Wu, Sheng-Ying]的文章
[Yu, Yan-Rong]的文章
[Cai, Yan]的文章
百度学术
百度学术中相似的文章
[Wu, Sheng-Ying]的文章
[Yu, Yan-Rong]的文章
[Cai, Yan]的文章
必应学术
必应学术中相似的文章
[Wu, Sheng-Ying]的文章
[Yu, Yan-Rong]的文章
[Cai, Yan]的文章
相关权益政策
暂无数据
收藏/分享
文件名: ebm%2E2011%2E011175.pdf
格式: Adobe PDF
此文件暂不支持浏览
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。