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IR@PKUHSC  > 北京大学第三临床医学院  > 内分泌科  > 期刊论文
学科主题: 临床医学
题名:
Homocysteine impairs coronary artery endothelial function by inhibiting tetrahydrobiopterin in patients with hyperhomocysteinemia
作者: He, Liyun2; Zeng, Hui2; Li, Fuwang3; Feng, Jieli2; Liu, Shan2; Liu, Jinbo2; Yu, Jie2; Mao, Jieming2; Hong, Tianpei1; Chen, Alex F.4; Wang, Xian3; Wang, Guang1,2
关键词: nitric oxide
刊名: AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
发表日期: 2010-12-01
DOI: 10.1152/ajpendo.00367.2010
卷: 299, 期:6, 页:E1061-E1065
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Endocrinology & Metabolism ; Physiology
研究领域[WOS]: Endocrinology & Metabolism ; Physiology
关键词[WOS]: NITRIC-OXIDE SYNTHASE ; OXIDATIVE STRESS ; FOLIC-ACID ; DYSFUNCTION ; DISEASE ; HUMANS ; ATHEROSCLEROSIS ; SECRETION ; MONOCYTES
英文摘要:

Hyperhomocysteinemia (HHcy) has been associated with impaired vascular endothelial function. Our previous study demonstrated significantly higher secretion of the chemokine monocyte chemoattractant protein-1 from monocytes in response to lipopolysaccharide in patients with HHcy. In the present study, we investigated whether coronary endothelial function was damaged in patients with chronic HHcy (plasma level of homocysteine > 15 mu mol/l) and, if so, whether this impaired endothelial function is induced by the uncoupling of endothelial nitric oxide synthase (eNOS). When tetrahydrobiopterin levels are inadequate, eNOS is no longer coupled to L-arginine oxidation, which results in reactive oxygen species rather than nitric oxide production, thereby inducing vascular endothelial dysfunction. The 71 participants were divided into two groups, control (n = 50) and HHcy (n = 21). Quantification of coronary flow velocity reserve (CFVR) was after rest and after adenosine administration done by noninvasive Doppler echocardiography. Plasma levels of nitric oxide and tetrahydrobiopterin were significantly lower in patients with HHcy than in controls (99.54 +/- 32.23 vs. 119.50 +/- 37.68 mu mol/l and 1.43 +/- 0.46 vs. 1.73 +/- 0.56 pmol/ml, all P < 0.05). Furthermore, CFVR was significantly lower in the HHcy than the control group (2.76 +/- 0.49 vs. 3.09 +/- 0.52, P < 0.05). In addition, plasma level of homocysteine was negatively correlated with CFVR. Chronic HHcy may contribute to coronary artery disease by inducing dysfunction of the coronary artery endothelium. The uncoupling of eNOS induced by HHcy in patients with chronic HHcy may explain this adverse effect in part.

语种: 英语
所属项目编号: 2006CB503802 ; 30728021 ; 30821001 ; 30770873 ; 2005-3013 ; 30728021
项目资助者: Major National Basic Research Program of China ; Chinese National Natural Science Foundation ; Capital Medicine Development Foundation ; Natural Sciences Foundation of China
WOS记录号: WOS:000285710400023
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/52823
Appears in Collections:北京大学第三临床医学院_内分泌科_期刊论文

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作者单位: 1.Peking Univ, Hlth Sci Ctr, Hosp 3, Dept Endocrinol, Beijing 100191, Peoples R China
2.Peking Univ, Dept Cardiovasc Med, Hosp 3, Beijing 100191, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Minist Educ, Sch Basic Med Sci,Key Lab Mol Cardiovasc Sci,Dept, Beijing 100191, Peoples R China
4.Univ Pittsburgh, Dept Surg, Sch Med & Vasc Surg Res, Pittsburgh, PA USA

Recommended Citation:
He, Liyun,Zeng, Hui,Li, Fuwang,et al. Homocysteine impairs coronary artery endothelial function by inhibiting tetrahydrobiopterin in patients with hyperhomocysteinemia[J]. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM,2010,299(6):E1061-E1065.
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