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血管紧张素转换酶(ACE)和血管紧张素转换酶2(ACE2)的多态性与高血压患者的体位性血压调节异常无关。

Polymorphisms of angiotensin-converting enzyme (ACE) and ACE2 are not associated with orthostatic blood pressure dysregulation in hypertensive patients.

作者信息

Fan Xiao-han, Wang Yi-bo, Wang Hu, Sun Kai, Zhang Wei-li, Song Xiao-dong, Cheng Jing-zhou, Wu Hai-ying, Zhou Xiang-liang, Hui Ru-tai

机构信息

Department of Cardiology and Hypertension Division, Ministry of Education, Cardiovascular Institute & FuWai Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China.

出版信息

Acta Pharmacol Sin. 2009 Sep;30(9):1237-44. doi: 10.1038/aps.2009.110. Epub 2009 Aug 17.

Abstract

AIM

The genetic background of orthostatic blood pressure dysregulation remains poorly understood. Since the renin-angiotensin system plays an important role in blood pressure regulation and response to position change, we hypothesized that angiotensin-converting enzyme (ACE) and ACE2 genetic polymorphisms might contribute, at least partially, to orthostatic blood pressure dysregulation in hypertensive patients.

METHODS

Two tag single nucleotide polymorphisms (SNPs) of ACE2 and ACE I/D were genotyped in 3630 untreated hypertensive patients and 826 normotensive subjects. Orthostatic hypertension was defined as an increase in systolic blood pressure of 20 mmHg or more and orthostatic hypotension as a drop in blood pressure of 20/10 mmHg or more within three minutes of assumption of upright posture.

RESULTS

Female and male patients had similar rates of orthostatic hypertension (16.5% vs 15.3%) and hypotension (22.5% vs 23.8%). No significant differences were detected in the minor allele frequency of ACE2 rs2106809, rs2285666, or ACE I/D in either female or male patients with orthostatic hypertension (15.1%, 22.7%, 19.6%, respectively), hypotension (13.8%, 25%, 16.5%), or normal orthostatic blood pressure response (14.4%, 21.9%, 15.8%) in additive, dominant or recessive models after adjustment for confounders (all P>0.05). The orthostatic changes in systolic and diastolic blood pressure were also comparable among patients carrying different genotypes. Similar results were observed in normotensive subjects.

CONCLUSION

These data provide no support for the involvement of ACE or ACE2 in the genetic predisposition to orthostatic hypotension or hypertension.

摘要

目的

体位性血压调节异常的遗传背景仍知之甚少。由于肾素-血管紧张素系统在血压调节和对体位变化的反应中起重要作用,我们推测血管紧张素转换酶(ACE)和ACE2基因多态性可能至少部分导致高血压患者的体位性血压调节异常。

方法

对3630例未经治疗的高血压患者和826例血压正常的受试者进行ACE2和ACE I/D的两个标签单核苷酸多态性(SNP)基因分型。体位性高血压定义为收缩压升高20 mmHg或更多,体位性低血压定义为在采取直立姿势后三分钟内血压下降20/10 mmHg或更多。

结果

女性和男性患者的体位性高血压(16.5%对15.3%)和低血压(22.5%对23.8%)发生率相似。在调整混杂因素后,无论是体位性高血压(分别为15.1%、22.7%、19.6%)、低血压(13.8%、25%、16.5%)或体位性血压反应正常(14.4%、21.9%、15.8%)的女性或男性患者中,ACE2 rs2106809、rs2285666或ACE I/D的次要等位基因频率在加性、显性或隐性模型中均未检测到显著差异(所有P>0.05)。携带不同基因型的患者收缩压和舒张压的体位性变化也相当。在血压正常的受试者中观察到类似结果。

结论

这些数据不支持ACE或ACE2参与体位性低血压或高血压的遗传易感性。

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