压力负荷性大鼠肥厚心肌中AngⅡ受体的表达

Expression of AngⅡ receptors in excess load-pressured hypertrophied cardiac muscles of rats

目的观察压力负荷性肥厚心肌中AngⅡ受体两种亚型AT1与AT2的表达变化及captopril干预对其表达的影响。方法选用腹主动脉缩窄方法制造压力负荷大鼠模型,观察压力负荷性大鼠心肌肥厚程度及心肌中AT1与AT2表达的变化。结果AC术后大鼠左室心肌肥大指数进行性加重,AC术后captopril干预可抑制心肌肥大发展;心肌中AC组心肌AT1受体的表达随AC的持续时间而不断上升,而AT2的表达仅在AC术后一过性增高,后随着左室负荷的持续而回降到对照水平,AT1/AT2值在AC术后1周时轻度升高,而后进行性降低;血管紧张素转换酶抑制剂(ACEI)AC术后干预在抑制心肌肥大发展的同时,显著抑制了心肌中的AT1表达,使AT1/AT2值显著回降。结论持续压力负荷增高引起心肌中AT1表达进行性增高,而对AT2的表达仅表现为早期一过性影响。ACEI干预可显著降低持续压力负荷性心肌中的AT1表达,从而有效阻止了AngⅡ通过AT1介导启动的心肌肥厚效应。

Objetive To study the effects of captopri on AT1 and AT2 receptors of load-pressured hypertrophied cardiac muscles of adult rats. Methods Using the methods of narrowing and contraction of the aorta of adult healthy rats to establish the model of animals with hypertrophied cardiac and to observe the changes of receptors AT1 and AT2 of hypertrophied cardiac muscles of AC rats by comprehensive applications of cardiac-tube, immunity tissue chemistry and the technique of image disjunction. Results Left ventricular and cardiac muscles of rats were increased remarkably as the pressure-loading time lasted. After using captopri, left ventricular hypertrophied one was decreased more significantly than that in control group. The expression of receptor AT 1 was increased remarkably as the pressure-loading time lasted. The expression of receptor AT2 was increased transiently, after that reached about as high as control group. AT1/AT2 was increased one week after operation, and then was progressively decreased. After AC, captopri prevented hypertrophied cardiac muscles and receptor AT1 in cardiac muscles. AT1/AT2 was remarkably decreased. Conclusion Load-pressured cardiac hypertrophy may increase the expression of AT1. The expression of receptor AT 2 was increased transiently. The main working mechanism of captopri＇s preventing and treating the load-pressured cardiac hypertrophy in adult rats may be lowering the expression of AT1 and may effectively block the cardiac hypertrophy regulation precess of Ang Ⅱ via AT1 preventing load-pressured cardiac hypertrophy in adult rats.