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血管紧张素转换酶基因插入/缺失多态性与阻塞性睡眠呼吸暂停之间的相互作用作为高血压的一种机制。

Interaction between the angiotensin-converting enzyme gene insertion/deletion polymorphism and obstructive sleep apnoea as a mechanism for hypertension.

作者信息

Boström Kristina Bengtsson, Hedner Jan, Melander Olle, Grote Ludger, Gullberg Bo, Råstam Lennart, Groop Leif, Lindblad Ulf

机构信息

Department of Clinical Sciences, Diabetes and Endocrinology, Skaraborg Institute, Skövde, Sweden.

出版信息

J Hypertens. 2007 Apr;25(4):779-83. doi: 10.1097/HJH.0b013e328017f6d5.

Abstract

OBJECTIVE

Obstructive sleep apnoea (OSA) confers a risk of hypertension and cardiovascular complications. Both the renin-angiotensin-aldosterone system and OSA are important determinants of blood pressure, but it is not fully known how they interact. The aim of this study was to explore the interaction between the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and OSA in the association with hypertension.

DESIGN

A community-based, case-control design with hypertensive patients in primary care (n = 157) and normotensive population controls (n = 181).

METHODS

All subjects underwent ambulatory polysomnography during one night. OSA was defined by a minimum of 10 apnoea/hypopnoea events per hour. Office blood pressure was measured and hypertension status was assessed. The genotypes were determined using polymerase chain reaction.

RESULTS

An interaction analysis including sex, ACE I/D polymorphism (DD and ID versus II), and OSA identified a significant interaction between OSA and the ACE I/D polymorphism: odds ratio (OR) 6.3, 95% confidence interval (CI) 1.8-22.5, P = 0.004 as well as between OSA and sex: OR 3.3, 95% CI 1.1-9.6, P = 0.033. OSA was significantly associated with hypertension in men but not in women.

CONCLUSION

The interaction between the ACE gene I/D polymorphism and OSA appears to be an important mechanism in the development of hypertension, particularly in men.

摘要

目的

阻塞性睡眠呼吸暂停(OSA)会增加患高血压和心血管并发症的风险。肾素 - 血管紧张素 - 醛固酮系统和OSA都是血压的重要决定因素,但它们之间如何相互作用尚不完全清楚。本研究的目的是探讨血管紧张素转换酶(ACE)基因插入/缺失(I/D)多态性与OSA在与高血压关联中的相互作用。

设计

一项基于社区的病例对照研究,研究对象为初级保健中的高血压患者(n = 157)和血压正常的人群对照(n = 181)。

方法

所有受试者在一个晚上进行动态多导睡眠图监测。OSA的定义为每小时至少10次呼吸暂停/低通气事件。测量诊室血压并评估高血压状态。使用聚合酶链反应确定基因型。

结果

一项包括性别、ACE I/D多态性(DD和ID与II相比)和OSA的交互分析发现,OSA与ACE I/D多态性之间存在显著交互作用:比值比(OR)为6.3,95%置信区间(CI)为1.8 - 22.5,P = 0.004;OSA与性别之间也存在显著交互作用:OR为3.3,95%CI为1.1 - 9.6,P = 0.033。OSA在男性中与高血压显著相关,而在女性中则不然。

结论

ACE基因I/D多态性与OSA之间的相互作用似乎是高血压发生发展的重要机制,尤其是在男性中。

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