早期运动训练延缓自发性高血压大鼠心脏病理变化的作用及机制  

Early exercise training postpones pathological alterations in heart of spontaneously hypertensive rats and its mechanisms

作　　者：洪玲[1] 赵晓霖 陈秀云[1] 林诚[1] 潘燕霞[1] 

机构地区：[1]福建医科大学医学技术与工程学院康复治疗学系,福建福州350004

出　　处：《中华高血压杂志》2016年第11期1034-1041,共8页Chinese Journal of Hypertension

基　　金：国家自然科学基金项目(81372111);福建省自然科学基金项目(2014J01339)

摘　　要：目的观察高血压前期有氧运动对自发性高血压大鼠(SHR)血压、心脏功能与结构以及心肌血管紧张素转换酶2(ACE2)信号通路的影响,探讨运动训练改善心脏病理变化的作用机制。方法 5周龄雄性SHR和正常血压大鼠(WKY)各24只,随机分成安静组(S)和运动训练组(E)。运动训练大鼠进行16周中低强度的跑台运动。运动结束,评估4组大鼠血压、左心室收缩和舒张功能、左心室肥厚和纤维化程度。实时荧光定量聚合酶链反应(realtime PCR)和Western blot分别检测左心室心肌ACE2、Mas受体mRNA和蛋白表达,酶联免疫吸附试验(ELISA)法检测左心室心肌组织血管紧张素(1-7)[Ang(1-7)]水平。结果 16周运动显著降低SHR收缩压(P<0.01)和左心室舒张末期内压(LVEDP)(P<0.01),增强左心室内压最大下降速率(P<0.01)。运动训练还降低SHR左心室质量(LVM)、心肌胶原容积分数(CVF)和血管周围胶原面积(PVCA)(均P<0.05),16周运动上调SHR左心室心肌ACE2和Mas受体mRNA和蛋白表达(均P<0.01),增加心肌Ang(1-7)水平(P<0.01)。16周运动不引起WKY左心室肥厚,但上调左心室心肌ACE2mRNA和Mas受体mRNA表达(均P<0.05)及Ang(1-7)水平(P<0.05)。结论高血压前期运动训练显著降低SHR血压、改善左心室功能并减轻心肌纤维化,其机制可能与运动增强心脏组织ACE2-Ang(1-7)-Mas轴功能有关。Objective To investigate the effects of aerobic exercise at prehypertension stage on the blood pressure, cardiac functions and pathological alterations as well as cardiac angiotensin converting enzyme 2 signaling in sponta- neously hypertensive rats （SHR）, and to elucidate the potential mechanisms. Methods Five-week-old male SHR （n：24） and normotensive Wistar Kyoto rats （WKY） （n=24）were randomly divided into sedentary （S） and exercise training （E） groups. The training rats ran on a treadmill at a low to middle intensity for 16 weeks. After comple- ted the exercise protocol, blood pressure, systolic and diastolic functions of the left ventricle, left ventricular hyper- trophy and fibrosis were evaluated. Real-time polymerase chain reaction （PCR） and Western blot were used to de- tect the mRNA and protein expressions of myocardial angiotensin converting enzyme 2 （ACE2） and Mas receptors, respectively. The angiotensin-（1-7） [Ang（1-7）] levels of the left ventricle were determined by enzyme linked im- munosorhent assay （ELISA）. Results 16-week exercise training significantly decreased systolic blood pressure （P〈0.01） and the left ventricular end diastolic pressure （LVEDP） （P〈0.01）, enhanced the maximal fall velocity of left ventricular pressure （- dp/dt=max ） （P〈0.01） in SHR. Exercise training also reduced the left ventricular mass （LVM）, the left ventricular collagen volume fraction （CVF） and perivascular collagen volume fraction （PVCA） in SHR （all P〈0.05）. 16-week exercise training greatly upregulated cardiac mRNA and protein expres- sions of ACE2 and Mas receptors （all P〈0.01 ） and increased myocardial level of Ang（1-7） （P〈0. 001） in SHR. In WKY, exercise training did not result in the hypertrophy of left ventricle, but upregulated the mRNA expression of ACE2 and Mas receptors of the left ventricle （all P〈0.05） and increased cardiac Ang（1-7） level （P〈0.05） in WKY. Conclusion Early exercise train

关 键 词：高血压 运动训练 血管紧张素转换酶2 MAS受体 心脏 

分 类 号：R544.1[医药卫生—心血管疾病]