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目的:探讨血管紧张素转换酶2(ACE2)和ACE基因多态性是否相互作用增加高血压发病易感性。方法:挑选ACE2基因的5个标签单核苷酸多态及ACE基因I/D多态性,采用标准的多聚酶链反应—限制性片段长度多态性技术进行基因分型,抽取部分测序验证。通过2组病例—对照研究[信阳:高血压病例973例(男性病例357例,女性病例616例)和对照969例(男性对照者355例,女性对照者614例);日照:病例286例(男性病例101例,女性病例185例)和对照316例(男性对照者126例,女性对照者190例)验证ACE2和ACE基因多态性与高血压的相关性。结果:ACE2基因rs2106809TT基因型和T等位基因分布频率在女性病例中显著高于女性对照者(OR:1.21,95%CI:1.09～1.34,P<0.001),差异有统计学意义;男性无统计学意义。未发现其它基因多态在两者间有统计学意义。Lo-gistic回归分析调整年龄、血脂、血糖等危险因素后,女性病例T等位基因携带者与女性对照者比较高血压易感性增加1.6倍(OR:1.59,95%CI:1.13～2.06,P<0.001),差异有统计学意义。女性病例ACEDD基因型+ACE2 rs2106809TT/TC基因型分布频率显著高于女性对照者(11.7%vs6.0%,P<0.001),差异有统计学意义。Logistic回归分析证实女性病例中ACE基因I/D与ACE2 rs2106809有交互作用(OR:1.25,95%CI:1.18～1.34,P<0.001),同时携带ACEDD中的ACE2 rs2106809TT/TC基因型者高血压危险增加(OR:2.75,95%CI:1.58～4.77,P<0.001),与对照者比较差异有统计学意义。上述结果在第二组病例对照研究中得到验证。结论:ACE2T等位基因是女性高血压的独立危险因素,ACEDD基因型增加这种危险。
Objective: To investigate whether angiotensin converting enzyme 2 (ACE2) and ACE gene polymorphism increase the susceptibility to hypertension. Methods: Five single nucleotide polymorphisms of ACE2 gene and ACE gene I / D polymorphism were selected and genotyped by standard polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Xinyang: 973 cases of hypertension (357 cases of male and 616 cases of female) and 969 cases of control (355 cases of male controls and 614 cases of female controls); sunshine: 286 cases (control group) 101 cases of male cases, 185 cases of female cases) and control 316 cases (126 cases of male controls, 190 cases of female controls) to verify ACE2 and ACE gene polymorphisms and hypertension correlation. Results: The frequencies of rs2106809TT genotype and T allele of ACE2 gene were significantly higher in women than in women (OR: 1.21, 95% CI: 1.09-1.34, P <0.001), and the difference was statistically significant Statistical significance. No other gene polymorphism was found between the two groups. Lo-gistic regression analysis adjusted for age, blood lipids, blood glucose and other risk factors, female patients with T allele carriers and female controls increased hypertension susceptibility 1.6 times (OR: 1.59,95% CI: 1.13 ~ 2.06, P <0.001), the difference was statistically significant. The frequency of ACEDD genotypes + ACE2 rs2106809TT / TC genotype in female cases was significantly higher than that in female controls (11.7% vs 6.0%, P <0.001). The difference was statistically significant. Logistic regression analysis confirmed that ACE gene I / D interacted with ACE2 rs2106809 in female patients (OR: 1.25, 95% CI: 1.18-1.34, P <0.001), while ACE2 rs2106809TT / TC genotype in ACEDD (OR: 2.75, 95% CI: 1.58 ~ 4.77, P <0.001), and the difference was statistically significant compared with the control group. The above results were validated in the second case-control study. CONCLUSION: The ACE2T allele is an independent risk factor for female hypertension and the ACEDD genotype increases this risk.