Expression of AngⅡ receptors in excess load-pressured hypertrophied cardiac muscles of rats
- VernacularTitle:压力负荷性大鼠肥厚心肌中AngⅡ受体的表达
- Author:
Xiaohong WANG
;
Jinjun LIU
;
Xingli SU
;
Guangdao GAO
- Publication Type:Journal Article
- Keywords:
captopril;
cardiac hypertrophy;
AT1 receptor;
AT2 receptor
- From:
Journal of Xi'an Jiaotong University(Medical Sciences)
1982;0(01):-
- CountryChina
- Language:Chinese
-
Abstract:
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 ll via AT1 preventing load-pressured cardiac hypertrophy in adult rats.
