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血管紧张素转换酶基因多态性与高血压病血管内皮纤溶障碍的关系
引用本文:赵杰娉,崔天祥,李莉,张强,张振香. 血管紧张素转换酶基因多态性与高血压病血管内皮纤溶障碍的关系[J]. 中国误诊学杂志, 2004, 4(1): 28-31
作者姓名:赵杰娉  崔天祥  李莉  张强  张振香
作者单位:1. 河南省胸科医院心内科,450003
2. 郑州大学第二附属医院,450003
摘    要:目的 :探讨 ACE基因 I/ D多态性与原发性高血压 (EH)及高血压血管内皮纤溶功能障碍间的关系。方法 :PCR检测 6 1例原发性高血压患者和正常对照组 2 8例的 ACE基因 I/ D多态性 ;发色底物法测 t- PA、PAI- 1活性 ,酶联免疫吸附双抗夹心法 (EL ISA)测 v WF含量。结果 :高血压组 DD基因型频率显著高于对照组 (P<0 .0 5 ) ,但 D等位基因频率分布在高血压组和正常组之间无差异性 (P>0 .0 5 )。高血压组 t- PA活性降低 ,PAI- 1活性、v WF含量升高 (P均 <0 .0 0 1)。高血压组 DD型 t- PA活性明显低于 ID、II型 (P<0 .0 0 1) ,而 ID、II型之间无统计学差异 (P>0 .0 5 ) ,DD型 PAI-1活性明显高于 ID、 型 (P<0 .0 0 1) ,而 ID、II型之间无统计学差异 (P>0 .0 5 ) ,v WF在 DD、ID、II型三者之间无明显差异 (P均 >0 .0 5 )。结论 :DD型是原发性高血压发病的危险因素。原发性高血压存在血管内皮损伤、纤溶功能障碍。t- PA、PAI- 1的变化与血管紧张素转换酶基因 I/ D多态性有关 ,DD基因型可引起纤溶功能紊乱。

关 键 词:高血压/酶学  高血压/病理生理学  肽基二肽酶A/遗传学  基因  多态现象(遗传学)  纤维蛋白溶解
文章编号:1009-6647(2004)01-0028-04
修稿时间:2003-11-03

Correlation of Angiotensin - Converting Enzyme Gene Insertion/Deletion Polymorphism with Fibrinolytic Dysfunction in Essential Hypertension
ZHAO Jie-ping,CUI Tian-xiang,LI Li,et al.. Correlation of Angiotensin - Converting Enzyme Gene Insertion/Deletion Polymorphism with Fibrinolytic Dysfunction in Essential Hypertension[J]. Chinese Journal of Misdiagnostics, 2004, 4(1): 28-31
Authors:ZHAO Jie-ping  CUI Tian-xiang  LI Li  et al.
Abstract:Objective:The experiment was designed to investigate the correlation of insertion/deletion polymorphism of ACE gene with essential hypertension as well as fibrinolytic dysfunction.Methods:We identified the ACE I/D polymorphism by PCR technique in 61 essential hypertension patients and 28 control subjects.Plasma t-PA, PAI-1 activities were measured by chromophoric substrate, the concentration of vWF was measured by Enzyme Linked Immunosorbent Assay (ELISA).Results:The DD genotype of ACE gene was significantly higher in essential hypertension groups than in control group (P<0.05), but D allele has no difference between the two groups. The markers of endothelium damage and fibrinolysis system dysfunction in essential hypertension group were higher significantly than control group: there were lower activity of t-PA, higher activity of PAI-1 and higher concentration of vWF in essential hypertension group than control group (all P< 0.001).The activity of t-PA in DD genotype was lower significantly than in ID or II genotype (P< 0.001), but there was no difference between ID and II (P> 0.05).The activity of PAI-1 in DD genotype was higher significantly than in ID or II genotype (P< 0.001), but there was no difference between ID and II (P> 0.05).The concentration of vWF did not differ among DD, ID and II genotype ( all P> 0.05).Conclusion:DD genotype was the risk factor of essential hypertension. There were endothelium damage and fibrinolysis dysfunction in essential hypertension.There was correlation between the variance of t-PA, PAI-1 and ACE I/D polymorphism, DD genotype could cause fibrinolysis dysfunction.
Keywords:Hypertension/enzymology  Hypertension/physiopathology  Peptidyl-dipeptidase A/genetics  Genes  Polymorphism(genetics)  Fibrinolysis
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