RAAS基因多态与男性原发性高血压患者不同强度有氧运动降压效果的关系

发布时间：2018-04-10 05:30

  本文选题：肾素-血管紧张素-醛固酮系统　切入点：基因多态　出处：《北京体育大学学报》2017年05期

【摘要】：目的:探讨肾素-血管紧张素-醛固酮系统(RAAS)基因多态与男性原发性高血压患者不同强度有氧运动降压效果的关系,为制定个性化运动处方提供依据。方法:78名男性原发性高血压患者利用聚合酶链式反应(PCR)测定血管紧张素转化酶(ACE)基因I/D、血管紧张素II 1型受体(AT1R)基因A/C和醛固酮合酶(CYP11B2)基因T/C多态。所有受试者分别以60%6)VO2max进行1次中等强度有氧运动实验(MAET)、以40%6)VO2max进行1次低强度有氧运动实验(LAET)以及1次安静对照实验(RCT),时间均为40min。每次实验前后测定24小时动态血压(ABP),包括收缩压(SBP)和舒张压(DBP)。结果:各基因型分布频率均符合哈-温遗传平衡定律(P0.05)。与实验前比较,MAET、LAET后各基因型组血压水平均显著性下降(P0.05),RCT后则无显著性变化(P0.05);LAET后,ACE-DD基因型组SBP低于ACE-II/ID基因型组(P0.05)。LAET后,≥3个RAAS高危等位基因组SBP和DBP均低于≤2个高危等位基因组(P0.05);MAET和RCT后,2组血压水平均无显著性差异(P0.05)。结论:RAAS基因多态可影响急性有氧运动的降压效应。ACE-DD基因型携带者低强度有氧运动的降压效果优于ACE-I等位基因(II/ID)者;≥3个RAAS高危等位基因患者低强度有氧运动的降压效果优于≤2个等位基因变异者;中等强度运动以及安静对照实验后,血压无显著性改变。
[Abstract]:Objective: to investigate the relationship between renin-angiotensin-aldosterone system (Ras) gene polymorphism and the antihypertensive effect of aerobic exercise with different intensity in male patients with essential hypertension.Methods Polymerase chain reaction (PCR) was used to determine the polymorphism of ACE-I / D, AP-1R and CYP11B2 gene in 78 male patients with essential hypertension.All subjects were given a moderate intensity aerobic exercise test with 60%6)VO2max, a low intensity aerobic exercise test with 40%6)VO2max, and a quiet control test for 40 mins.Before and after each experiment, ambulatory blood pressure (ABP) and diastolic blood pressure (DBP) were measured at 24 hours, including systolic blood pressure (SBP) and diastolic blood pressure (DBP).Results: the distribution frequency of all genotypes was in accordance with the law of ha-temperature genetic balance (P0.05A).There was no significant change in the blood pressure level of each genotype group after RCT compared with that before the experiment. The SBP in the ACE-DD genotype group was lower than that in the ACE-II/ID genotype group (P 0.05).There was no significant difference in blood pressure levels between the two groups after RCT and P0.05 alleles (P 0.05), the genomic SBP and DBP of 鈮，

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