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冠心病患者血浆内皮素 -1和血管加压素水平与人类血管紧张素I转换酶基因的插入/缺失多态性无关。

Endothelin-1 and vasopressin plasma levels are not associated with the insertion/deletion polymorphism of the human angiotensin I-converting enzyme gene in patients with coronary artery disease.

作者信息

Al-Fakhri N, Linhart R E, Philipp M, Heidt M, Hehrlein F W, Gardemann A, Katz N

机构信息

Instritute of Clinical Chemistry and Pathobiochemistry, Justus Liebig University, Gaffkystrasse 11, 35392 Giessen, Germany.

出版信息

J Hum Hypertens. 2003 Feb;17(2):133-8. doi: 10.1038/sj.jhh.1001519.

Abstract

The objective was to investigate whether the renin-angiotensin (RA) system and related peptides endothelin-1 (ET-1) and vasopressin (VP) influence the development of coronary artery disease (CAD). Angiotensin I-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism has been associated with the risk of CAD. The ACE I/D polymorphism determines ACE activity, but plasma levels of other RA system components remain unchanged. However, ET-1 and VP production could be increased by RA system-dependent stimulation, continually promoted by paracrine stimulation and sustained by neointimal growth. ET-1 and VP have not been associated with the ACE I/D polymorphism so far. The present study investigated the association of the ACE I/D polymorphism with plasma concentrations of ET-1 and VP, as well as with renin, angiotensin-II (AT-II) and ACE activity in 98 Caucasian individuals with CAD. ACE I/D polymorphism showed no association with plasma levels of VP, ET-1, AT-II or renin. These parameters were also not associated taking into consideration different patient variables, such as diabetes mellitus, hypertension or severity of CAD. Only plasma ACE activity was associated with the D allele. In conclusion, the ACE I/D polymorphism could not be related to plasma concentrations of VP, ET-1, renin or AT-II, but as previously demonstrated, it could only be related to ACE activity in patients with CAD. Differences in ACE activity between ACE I/D genotype subgroups are probably compensated within the RA system itself or within non-ACE pathways, so that plasma concentrations of the related peptides ET-1 and VP remain unaffected.

摘要

目的是研究肾素 - 血管紧张素(RA)系统以及相关肽内皮素 -1(ET -1)和血管加压素(VP)是否影响冠状动脉疾病(CAD)的发展。血管紧张素I转换酶(ACE)插入/缺失(I/D)基因多态性与CAD风险相关。ACE I/D多态性决定ACE活性,但RA系统其他成分的血浆水平保持不变。然而,ET -1和VP的产生可通过RA系统依赖性刺激增加,由旁分泌刺激持续促进,并由新生内膜生长维持。迄今为止,ET -1和VP与ACE I/D多态性无关。本研究调查了98名患有CAD的白种人个体中ACE I/D多态性与ET -1和VP血浆浓度以及肾素、血管紧张素II(AT -II)和ACE活性之间的关联。ACE I/D多态性与VP、ET -1、AT -II或肾素的血浆水平无关。考虑到不同的患者变量,如糖尿病、高血压或CAD严重程度,这些参数也无关联。仅血浆ACE活性与D等位基因相关。总之,ACE I/D多态性与VP、ET -1、肾素或AT -II的血浆浓度无关,但如先前所示,它仅与CAD患者的ACE活性相关。ACE I/D基因型亚组之间ACE活性的差异可能在RA系统自身或非ACE途径内得到补偿,从而使相关肽ET -1和VP的血浆浓度不受影响。

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