Circulation, Vol 89, 2198-2203, Copyright © 1994 by American Heart Association
H Ito, M Hiroe, Y Hirata, H Fujisaki, S Adachi, H Akimoto, Y Ohta and F Marumo
BACKGROUND: We have recently shown that angiotensin II-induced hypertrophy
of cultured rat cardiomyocytes was partially blocked by an endothelin (ET)
receptor antagonist (BQ123) selective for the ETA subtype, suggesting the
possible involvement of endogenous ET-1 in the mechanism of cardiac
hypertrophy in vitro. In the present study, we studied the in vivo blockade
effects of BQ123 on cardiac hypertrophy provoked by left ventricular
overload with aortic banding in adult rats. METHODS AND RESULTS: Forty rats
were divided into four groups: (1) sham-operated rats without BQ123
administration, (2) rats with aortic banding without BQ123 administration,
(3) sham-operated rats with BQ123 administration, and (4) rats with aortic
banding with BQ123 administration. BQ123 (250 micrograms/h) was
administered continuously by an osmotic pump starting 24 hours before
operation. BQ123 blocked increases in the ratio of left ventricular weight
to body weight and in the diameter of cardiomyocytes provoked by aortic
banding at 1 week, but those blockade actions were no longer observed at 2
weeks. Skeletal alpha-actin and atrial natriuretic peptide (ANP) mRNA in
the left ventricle, transcriptional markers for cardiac hypertrophy,
significantly increased in the rats with aortic banding at 1 week and 2
weeks. In the rats with BQ123 administration, despite the hemodynamic
overload, skeletal alpha-actin and ANP mRNA in the left ventricle remained
at the control levels at 1 week; however, those blockade actions were
abolished at 2 weeks. Plasma ET-1 levels increased after aortic banding,
peaking at 24 hours, then returned to the basal level at 4 days.
Prepro-ET-1 mRNA levels in the left ventricle also increased 24 hours after
aortic banding, then declined to the basal level at 4 days. CONCLUSIONS:
These data suggest that endogenous ET-1 synthesized in the cardiovascular
system plays a role in the mechanism of cardiac hypertrophy during the
early phase of pressure overload in vivo.
ARTICLES
Endothelin ETA receptor antagonist blocks cardiac hypertrophy provoked by hemodynamic overload
Second Department of Internal Medicine, Tokyo Medical and Dental University, Japan.
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