论文部分内容阅读
Objective. In a model of rat cardiac hypertrophy, the changes in the distribution of ET- 1 receptors in two subcellular fractions, the sarcolemma and the light vesicles during myocardial hypertrophy were studied. Methods. Cardiac hypertrophy was produced by placing a constricting clip around the suprarenal abdominal aorta of rats, and ET- 1 receptor was assayed with radioactive analysis method. Results. It was found that plasma and ventricular ET- 1 levels increased significantly on week 2 and week 4 of pressure overload. ET- 1 binding studies showed that during myocardial hypertrophy, the maximum binding capacity (Bmax) was increased by 41% (P< 0.01) and 65% (P< 0.01) in sarcolemma in H- 2 week and H- 4 week groups, but was decreased by 24% (P< 0.01) and 21% (P< 0.01) in light vesicles. The sum of Bmax of sarcolemmal and light vesicle fractions was increased by 33% (P< 0.01) and 57% (P< 0.01) in group H- 2 week and H- 4 week, respectively. Conclusion. ET- 1 receptors in rat heart were externalized from light vesicles to sarcolemma, which may contribute to the development of myocardial hypertrophy.
Objective. In a model of rat cardiac hypertrophy, the changes in the distribution of ET-1 receptors in two subcellular fractions, the sarcolemma and the light vesicles during myocardial hypertrophy were studied. Methods. Cardiac hypertrophy was produced by placing a constricting clip around the Results were found that plasma and ventricular ET-1 levels increased significantly on week 2 and week 4 of pressure overload. ET-1 binding studies showed that during myocardial hypertrophy, the maximum binding capacity (Bmax) was increased by 41% (P <0.01) and 65% (P <0.01) in sarcolemma in H- 2 week and H- 4 weeks groups, but was decreased by 24% The sum of Bmax of sarcolemmal and light vesicle fractions was increased by 33% (P <0.01) and 57% (P <0.01) in group H-2 weeks (P <0.01) and H-4 weeks, respectively. Conclusion. ET-1 receptors in rat heart were externallyized from light vesicles to sarcolemma, which may contribute to the development of myocardial hypertrophy.