摘要
目的探讨内皮型一氧化氮合酶(eNOS)基因G894T多态性与替米沙坦降压效果的相关性。方法轻、中度原发性高血压(以下简称高血压)患者75例服替米沙坦单药4周,观察临床疗效,并采用多聚酶链式反应-限制性内切酶片段长度多态性方法(PCR-RFLP)分析患者eNOS基因G894T的基因型。结果高血压患者eNOS基因G894T3种基因型分别为GG44.0%、GT41.3%、TT14.7%,其中G、T等位基因频率分别为64.7%和35.3%。治疗前GG+GT基因型组和GG基因型组患者的收缩压、舒张压和平均动脉压比较差异均无统计学意义。治疗4周后,GT+TT基因型组患者舒张压下降的幅度〔(6.1±7.3)mmHg(1mmHg=0.133kPa)〕大于GG基因型组〔(4.0±8.0)mmHg〕,但差异无统计学意义(P=0.624),收缩压下降的幅度〔(7.7±12.8)mmHg〕比GG基因型组〔(9.6±19.0)mmHg〕小,差异亦无统计学意义(P=0.623)。结论在本组高血压人群中未发现eNOS基因G894T多态性与血管紧张素Ⅱ受体拮抗剂替米沙坦类药物降压效果的相关性。
Objective To investigate the association of the G894T polymorphism of endothelial nitric oxide synthase(eNOS) gene with the antihypertensive effects of telmisartan in essential hypertensive patients. Methods Seventy-five patients with mild to moderate essential hypertension diagnosed according to criteria of hypertension of WHO/ISH were enrolled in and treated with telmisartan for 4 weeks. Polymerase chain reaction combined with restrictive enzyme digestion was used to detect the G894T polymorphisms of eNOS gene in patients. Results There are three genotype-GG, GT, TT( their genotype frequencies is respectively 44.0% , 41.3% , 14.7% ) , the frequency of G allele is 64.7% and T allele is 35.3%. Before treatment, There is no statistically significant in SBP or DBP or MAP between GG genotype patients and GT + TT genotype patients; After 4-weeks' treatment of telmisartan, the decrease of DBP with GT + TT genotype patients [ (6.1 ±7.3)mmHg ( 1 mmHg =0. 133 kPa) ]was higher than that of GG genotype[ (4.0 ±8.0)mmHg], but it is not statistically significant (P = 0.624) ; however, the decrease of S BP with GG genotype patients [ (9.6 ± 19.0)mmHg ] was higher than that of GT+TT genotype[ (7.7± 12.8)mmHg] ,but it is not statistically significant(P =0.623). Conclusion We can not found that the association of eNOS gene G894T polymorphisms with antihypertensive effects of telmisartan in this selected hypertensive patients.
出处
《首都医科大学学报》
CAS
2007年第1期107-109,共3页
Journal of Capital Medical University
关键词
原发性高血压
内皮型一氧化氮合酶
多态性
essential hypertension
gene polymorphism
antihypertensive effects