Miao Chao-Yu, Zhang Li-Ming, Yuan Wen-Jun, Su Ding-Feng
Department of Pharmacology, Basic Medical College, Second Military Medical University, Shanghai 200433, China.
Acta Pharmacol Sin. 2003 Aug;24(8):812-8.
Angiotensin II and AT1 receptor are the major effector components of renin-angiotensin system (RAS), and also the main growth-stimulating factors in cardiovascular system. The present study was to observe these two factors in the hypertrophied ventricles and aortas of sinoaortic-denervated rats.
Rats were examined at 2, 10, and 16 weeks after sinoaortic denervation (SAD). The hypertrophy was evaluated by the ratio of organ weight to body weight. Angiotensin II concentration and AT1 receptor mRNA expression were measured by radioimmunoassay and RT-PCR respectively, using a positive control of candesartan treatment.
Aortic hypertrophy existed in 2-, 10-, and 16-week SAD rats, left ventricular hypertrophy in 10- and 16-week SAD rats, and right ventricular hypertrophy in 16-week SAD rats. In all three kinds of examined SAD rats, plasma angiotensin II levels remained unchanged, indicating circulating RAS is at normal level in the chronic phase of SAD. However, cardiovascular tissue RAS was activated, as evidenced by increase of aortic angiotensin II concentrations at 10 and 16 weeks after SAD, and up-regulation of aortic and left ventricular AT1 receptor mRNA expressions at 16 weeks after SAD.
The activated tissue RAS is secondary to the hypertrophy, and probably involved in the maintenance of cardiovascular hypertrophy following SAD.
血管紧张素II和AT1受体是肾素-血管紧张素系统（RAS）的主要效应成分，也是心血管系统中主要的生长刺激因子。本研究旨在观察去窦弓神经大鼠肥厚心室和主动脉中的这两种因子。
在去窦弓神经（SAD）后2周、10周和16周对大鼠进行检查。通过器官重量与体重之比评估肥厚程度。分别采用放射免疫分析法和RT-PCR法测定血管紧张素II浓度和AT1受体mRNA表达，并以坎地沙坦治疗作为阳性对照。
2周、10周和16周的SAD大鼠存在主动脉肥厚，10周和16周的SAD大鼠存在左心室肥厚，16周的SAD大鼠存在右心室肥厚。在所有三种检查的SAD大鼠中，血浆血管紧张素II水平保持不变，表明在SAD慢性期循环RAS处于正常水平。然而，心血管组织RAS被激活，SAD后10周和16周主动脉血管紧张素II浓度增加以及SAD后16周主动脉和左心室AT1受体mRNA表达上调证明了这一点。
激活的组织RAS继发于肥厚，可能参与SAD后心血管肥厚的维持。
