论文部分内容阅读
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 observe the effect of prehypertensive aerobic exercise on blood pressure, cardiac function and structure and cardiac angiotensin-converting enzyme 2 (ACE2) signaling in spontaneously hypertensive rats (SHR), and to explore the mechanism of exercise training in improving cardiac pathological changes . Methods A total of 24 male Wistarder SHR and normal Wistar rats (WKY), each of 5 weeks old, were divided into quiet group (S) and exercise training group (E) randomly. Exercise training rats for 16 weeks in low-intensity treadmill exercise. After the exercise, blood pressure, left ventricular systolic and diastolic function, left ventricular hypertrophy and fibrosis were evaluated in the four groups. Real-time PCR and Western blot were used to detect mRNA and protein expression of ACE2 and Mas receptor in left ventricular myocardium. ELISA was used to detect the expression of angiotensin (1-7) in left ventricular myocardium ) [Ang (1-7)] level. Results 16-week exercise significantly reduced the systolic pressure of SHR (P <0.01) and left ventricular end-diastolic pressure (LVEDP) (P <0.01), and increased the maximum rate of decline of left ventricular pressure (P <0.01). Exercise training also reduced left ventricular mass (LVM), myocardial collagen volume fraction (CVF) and perivascular collagen area (PVCA) of SHR (both P <0.05) (All P <0.01), and increased the level of Ang (1-7) in myocardium (P <0.01). 16-week exercise did not cause left ventricular hypertrophy in WKY, but up-regulated ACE2 mRNA and Mas receptor mRNA (all P <0.05) and Ang (1-7) in left ventricular myocardium (P <0.05). Conclusions Prehypertension exercise training can significantly reduce SHR blood pressure, improve left ventricular function and reduce myocardial fibrosis. The mechanism may be related to exercise-enhanced cardiac ACE2-Ang (1-7) -Mas axis function.