Li Xin, Wang Kun
Department of Physical Education, Chengdu University, Chengdu, Sichuan 610106, P.R. China.
Department of Physical Education, Shanghai Jiao Tong University, Shanghai 200240, P.R. China.
Mol Med Rep. 2017 Sep;16(3):2439-2444. doi: 10.3892/mmr.2017.6864. Epub 2017 Jun 27.
The current study was aimed at examining the effects of moderate‑intensity endurance exercise on the expression of angiotensin II (AngII) and AngII type 1 receptor (AT1R) in the rat heart. Male Sprague‑Dawley rats were randomly divided into the control group (n=20) and moderate‑intensity endurance exercise group (n=20). Cardiac hypertrophy was induced by treadmill endurance training for 8 weeks. The mRNA expression of AngII and AT1R were assessed by reverse transcription‑quantitative polymerase chain reaction. The immune response positive area and optical density of AngII and AT1R was measured by immunohistochemistry. AngII was primarily expressed in the cytoplasm and membrane, however infrequently in coronary vascular wall smooth muscle cells. AT1R was primarily expressed in the coronary vessel wall smooth muscle, rarely in cardiac cells. The mRNA expression of cardiac AngII was significantly increased after the 8‑week exercise period, while AT1R was significantly decreased. Immunohistochemistry indicated a significant increase in the AngII immune‑positive area and optical density after the 8‑week exercise. The AT1R immune‑positive area and optical density was significantly reduced following the 8‑week exercise. In conclusion, subsequent to 8‑weeks endurance training, the AngII expression was increased and the AT1R expression was decreased. AT1R may expand the coronary artery, thereby increasing coronary blood flow and ensuring the energy supply of heart during exercise. The expression change in AngII does not reflect the character of cardiac hypertrophy. The exercise‑induced change in the expression of AngII and AT1R may be a protective mechanism to avoid cardiac pathological hypertrophy.
本研究旨在探讨中等强度耐力运动对大鼠心脏中血管紧张素II（AngII）及血管紧张素II 1型受体（AT1R）表达的影响。将雄性Sprague-Dawley大鼠随机分为对照组（n = 20）和中等强度耐力运动组（n = 20）。通过跑步机耐力训练8周诱导心脏肥大。采用逆转录-定量聚合酶链反应评估AngII和AT1R的mRNA表达。通过免疫组织化学测量AngII和AT1R的免疫反应阳性面积和光密度。AngII主要表达于细胞质和细胞膜，在冠状动脉血管壁平滑肌细胞中较少见。AT1R主要表达于冠状动脉血管壁平滑肌，在心肌细胞中少见。8周运动期后，心脏AngII的mRNA表达显著增加，而AT1R显著降低。免疫组织化学显示，8周运动后AngII免疫阳性面积和光密度显著增加。8周运动后，AT1R免疫阳性面积和光密度显著降低。总之，8周耐力训练后，AngII表达增加，AT1R表达降低。AT1R可能扩张冠状动脉，从而增加冠状动脉血流量并确保运动期间心脏的能量供应。AngII表达的变化并不反映心脏肥大的特征。运动诱导的AngII和AT1R表达变化可能是一种避免心脏病理性肥大的保护机制。
