Polymorphism in endothelin-related genes limits exercise-induced decreases in arterial stiffness in older subjects
Polymorphism in endothelin-related genes limits exercise-induced decreases in arterial stiffness in older subjects
复制标题
DOI：
10.1161/01.hyp.0000217520.44176.73
复制
发表时间：
2006-05-01
期刊：
影响因子：
8.3
通讯作者：
Matsuda, M
中科院分区：
文献类型：
--
作者：
Iemitsu, M;Maeda, S;Matsuda, M
动脉硬化的增加与衰老有关，这可以通过定期锻炼来改善。内皮素（ET）系统在调节血管张力和动脉粥样硬化的发展中起着重要作用。我们假设ET相关基因的分子变异（即基因多态性）可能影响人类受试者运动诱导的动脉僵硬度随年龄的改善。本研究对191名健康的中老年人（65 ± 1岁）进行了横断面调查，以阐明有规律的运动诱导的动脉僵硬度改善与ET转换酶（ECE）- 1、ECE- 2、ET- A受体（ET- A）和ET- B受体（ET- B）基因多态性之间的关系.根据能量消耗的中位数（186千卡/天），将研究对象分为活动组和非活动组。肱踝动脉脉搏波传导速度（baPWV）用于评估动脉僵硬度. ET系统4种不同的多态性基因分型：ECE- 1第17内含子2013（+ 289）A/ G，ECE- 2第5内含子669（+ 17）T/ C，ET- A第6外显子958 A/ G，ET- B第4外显子831 A/ G。活性组的基线baPWV显著降低，血压无任何变化。ECE- 1基因多态性影响基础血压。ECE- 1和ECE- 2基因多态性对活动组和非活动组的baPWV无影响。而ET- A和ET- B基因多态性均影响两组baPWV.本研究结果提示，ET- A和ET- B多态性的差异可能影响血管壁对运动的反应，而ECE- 1多态性可能影响基础血压。
Increase in arterial stiffness is associated with aging, which is improved by regular exercise. Endothelin ( ET) system has crucial roles in regulating vascular tone and in the progression of atherosclerosis. We hypothesized that molecular variations ( ie, gene polymorphisms) in ET- related gene might affect exercise- induced improvement in arterial stiffness with age in human subjects. The present study provides a cross- sectional investigation of 191 healthy middle- aged and older ( 65 +/- 1 years) human subjects to clarify the relationship between the regular exercise- induced improvement of arterial stiffness and the gene polymorphisms of ET converting enzyme ( ECE)- 1, ECE- 2, ET- A receptor ( ET- A), and ET- B receptor ( ET- B). The study subjects were divided into active and inactive groups based on the median value ( 186 kcal/ d) of energy expenditure. Brachial- ankle arterial pulse wave velocity ( baPWV) was used to evaluate arterial stiffness. All individuals were genotyped for 4 different polymorphisms of the ET system: 2013( + 289) A/ G in intron 17 of ECE- 1, 669( + 17) T/ C in intron 5 of ECE- 2, 958A/ G in exon 6 of ET- A, and 831A/ G in exon 4 of ET- B. The baseline baPWV was significantly lower in the active group without any change in blood pressure. Polymorphisms in ECE- 1 influenced basal blood pressure. Polymorphisms in ECE- 1 and ECE- 2 had no effect on baPWV between active and inactive groups. However, polymorphisms in both ET- A and ET- B affected baPWV in the 2 groups. The present results suggest that differences in ET- A and ET- B polymorphisms may influence the response of the vascular wall to exercise whereas ECE- 1 polymorphisms may affect basal blood pressure.