| Essential hypertension is one of the most common cardiovascular diseases in China. The research of epidemiology has found that there is a increasing tendency in late 30 years. The mechanism of essential hypertension has been put more and more attention. Essential hypertension is regarded as a multigenic hereditary disease now, one third of the variance of blood pressure is caused by hereditary factor. The correlative gene is the focal point in hereditary research of essential hypertension. Renin-angiotensin System (RAS) plays an important role in the adjustment of blood pressure, water and electrolyte, Angiotensin-converting enzyme (ACE) is one of the important parts of it, so, the researches of ACE gene have been done profoundly. But no uniform conclusions have been drawn.In the process of studying the mechanism of essential hypertension, endothelial cell is gradually paid more attention to. Vascular endothelialcell is regarded as having many physiological functions, it plays an important role in regulating vascular tension and the growth of vascular smooth muscle, maintaining the balance of coagulation-fibrinolysis system, adjusting the coherence between endothelial cell and inflammatory cell, inhibiting platelet agglutination. So, the variance of endothelial cell function is becoming focal point in the research of mechanism of essential hypertension. It has been found that there is endothelial dysfunction in hypertension. But its hereditary mechanism is not very clearly. Object i ve:The experiment was designed to investigate the correlation of insertion/deletion polymorphism of ACE gene with essential hypertension as well as fibrinolytic dysfunction through measuring the activities of t-PA, PAI-1 and the concentration of vWF in 61 essential hypertension patients and 28 control subjects. Furthermore, we can explore the pathogenesis of essential hypertension in the level of molecular biology and give help to clinical diagnosis and prevention of complication. Methods:61 essential hypertension patients and 28 control subjects were recruited in this study. There were no statistic difference between two groups in age and sex. All these samples were extracted DNA by UNIQ-10 column genome DNA extracting reagent box and identified the ACE I/D polymorphism by PCR technique, measurement of serum markers: plasma t-PA, PAI-1 activities were measured by chromophoric substrate, the concentration of vWF was measured by Enzyme Linked Immunosorbent Assay (ELISA). ResuIts: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 damageand 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). Cone I us i on:1. There was correlation between ACE I/D polymorphism and the risk of essential hypertension as well as pathogenesis. DD genotype was the risk factor of essential hypertension.2. There were endothelium damage and fibrinolysis dysfunction: lower activity of t-PA; higher activity of PAI-1 and higher concentration of vWF.3. There was correlation between the variance of t-PA, PAI-1 and ACE I/D polymorphism, DD genotype could cause fibrinolysis dysfunction.4. The relationship between ACE I/D polymorphism and the variance concentration of vWF had not proved.
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