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目的研究血管紧张素II-1型受体(AngiogenesisIIType1Receptor,AT1R)基因1166位点多态性与原发性高血压(EssentialHypertension,EH)的关系和血浆一氧化氮(NitricOxide,NO)、内皮素(Endothelin,ET)在EH发病中的相关性。方法采用聚合酶链反应、限制性内切酶酶解及电泳分型的方法对AT1R基因1166位点的多态性进行分析,硝酸还原酶法和放射免疫法分别测定两组血浆NO、ET值。结果①EH组中1166C等位基因频率显著高于对照组(P<0.05)。②EH组与对照组比较NO活性降低;ET水平升高(P<0.001)。③EH组中CC型血浆NO水平明显低于AC型(P<0.01);血浆NO、ET水平在AA、AC型之间无显著性差异(P<0.05)。结论①AT1R基因1166位点多态性与EH相关,1166C等位基因是EH发病的危险因素。②EH组存在血管内皮舒缩功能障碍,表现为血浆NO浓度降低、ET浓度升高。③EH血管内皮功能障碍与AT1R基因A1166C多态性有关,1166CC基因型可导致血管内皮舒缩功能障碍,提示EH血管内皮功能障碍可能存在遗传机制。④血浆NO水平与EH发病危险呈负相关;而血浆ET浓度升高是EH发病的危险因素。
Objective To investigate the relationship between 1166 polymorphism of angiotensin Ⅱ type 1 receptor (AT1R) gene and Essential Hypertension (EH) and the relationship between Nitric Oxide (NO) and Endothelin Endothelin, ET) in the pathogenesis of EH. Methods Polymorphisms of AT1R gene at position 1166 were analyzed by polymerase chain reaction, restriction endonuclease digestion and electrophoresis typing. Nitric oxide reductase and radioimmunoassay were used to determine plasma NO and ET . Results ① The frequency of 1166C allele in the EH group was significantly higher than that in the control group (P <0.05). ② Compared with control group, NO activity decreased and ET level increased in EH group (P <0.001). ③ The level of NO in CC group was significantly lower than that in AC group in EH group (P <0.01). There was no significant difference in plasma NO, ET level between AA and AC genotypes (P <0.05). Conclusion ① 1166 polymorphism of AT1R gene is associated with EH, and 1166C allele is a risk factor of EH. ②EH group has vascular endothelial systolic dysfunction, manifested as decreased plasma concentrations of NO, ET increased. ③EH vascular endothelial dysfunction and AT1R gene A1166C polymorphism, 1166CC genotype can lead to vascular endothelial systolic dysfunction, suggesting that EH vascular endothelial dysfunction may exist genetic mechanisms. ④ The level of NO in plasma was negatively correlated with the risk of EH. The increased plasma ET was the risk factor of EH.