Intracellular redistribution of cardiac endothelin-1 receptor in rat during 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 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 (B(max)) 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 B(max) 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.


CONCLUSIONS
ET-1 receptors in rat heart were externalized from light vesicles to sarcolemma, which may contribute to the development of myocardial hypertrophy.
Wang
X
X
Institute of Cardiovascular Research, First Hospital of Peking University, Beijing 100034.
Qi
Y
Y
Yang
J
J
Tong
L
L
Pang
Y
Y
Tang
C
C
D000818:Animals; D006332:Cardiomegaly / Q000378:metabolism*; D006352:Heart Ventricles; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D044022:Receptor, Endothelin A / Q000378:metabolism*; D012508:Sarcolemma / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000378:metabolism
D044022:Receptor, Endothelin A