INTRACELLULAR REDISTRIBUTION OF CARDIAC ENDOTHELIN- 1 RECEPTOR IN RAT DURING MYOCARDIAL HYPERTROPHY
中国医学科学杂志(英文版)2001年0卷第2期 页码:86-92
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INTRACELLULAR REDISTRIBUTION OF CARDIAC ENDOTHELIN- 1 RECEPTOR IN RAT DURING MYOCARDIAL HYPERTROPHY
Affiliations:
Author bio:
Funds:
the National Major Basic Research Program(No.G2000056905)
DOI:
中图分类号:R363
纸质出版日期:2001
Accepted:
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INTRACELLULAR REDISTRIBUTION OF CARDIAC ENDOTHELIN- 1 RECEPTOR IN RAT DURING MYOCARDIAL HYPERTROPHY[J]. 中国医学科学杂志(英文版), 2001,0(2):86-92.
INTRACELLULAR REDISTRIBUTION OF CARDIAC ENDOTHELIN- 1 RECEPTOR IN RAT DURING MYOCARDIAL HYPERTROPHY[J]. Chinese medical sciences journal, 2001, 0(2): 86-92.
INTRACELLULAR REDISTRIBUTION OF CARDIAC ENDOTHELIN- 1 RECEPTOR IN RAT DURING MYOCARDIAL HYPERTROPHY[J]. 中国医学科学杂志(英文版), 2001,0(2):86-92.DOI:
INTRACELLULAR REDISTRIBUTION OF CARDIAC ENDOTHELIN- 1 RECEPTOR IN RAT DURING MYOCARDIAL HYPERTROPHY[J]. Chinese medical sciences journal, 2001, 0(2): 86-92.DOI:
INTRACELLULAR REDISTRIBUTION OF CARDIAC ENDOTHELIN- 1 RECEPTOR IN RAT DURING MYOCARDIAL HYPERTROPHY
摘要
Abstract
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.