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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(P>0.05)。与实验前比较,MAET、LAET后各基因型组血压水平均显著性下降(P<0.05),RCT后则无显著性变化(P>0.05);LAET后,ACE-DD基因型组SBP低于ACE-II/ID基因型组(P<0.05)。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(P<0.05);MAET和RCT后,2组血压水平均无显著性差异(P>0.05)。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。
Objective: To investigate the relationship between renin - angiotensin - aldosterone system (RAAS) gene polymorphism and different intensity aerobic exercise antihypertensive effect in male patients with essential hypertension, and to provide basis for formulating personalized exercise prescription. Methods: A total of 78 patients with essential hypertension were enrolled in this study. ACE gene I / D, AT1R A / C, and Angiotensin converting enzyme 1 receptor were detected by polymerase chain reaction (PCR) Aldosterone synthase (CYP11B2) gene T / C polymorphism All subjects underwent one moderate aerobic exercise test (MAET) at 60% 6) VO2max, one low intensity aerobic exercise test (LAET) at 40% 6) VO2max, and one quiet control trial (RCT ), The time is 40min. 24 hours ambulatory blood pressure (ABP), including systolic blood pressure (SBP) and diastolic blood pressure (DBP), was measured before and after each experiment. Results: The distribution frequency of each genotype accorded with the law of genetic equilibrium of ha-temperature (P> 0.05). Compared with those before the experiment, the blood pressure levels of all genotypes decreased significantly after MAET and LAET (P <0.05), but no significant changes after RCT (P> 0.05). After LAET, the SBP of ACE-DD genotype was lower than ACE-II / ID genotype group (P <0.05). After LAET, SBP and DBP of ≥3 high risk alleles of RAAS were all lower than ≤2 high risk alleles (P <0.05). After MAET and RCT, there was no significant difference in BPP between the two groups (P> 0.05). Conclusion: RAAS gene polymorphism can affect the antihypertensive effect of acute aerobic exercise. ACE-DD genotype carriers have lower antihypertensive effect than ACE-I allele (II / ID) in low-intensity aerobic exercise. The antihypertensive efficacy of low-intensity aerobic exercise in ≥3 RAAS high-risk allele patients is superior No significant changes in blood pressure after ≤ 2 allelic variations in moderate-intensity exercise and in quiescent control trials.