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Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, and Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R2H 2A6
Alterations in general
characteristics and morphology of the heart, as well as changes
in hemodynamics, myosin heavy chain isoforms, and 
-adrenoceptor
responsiveness, were determined in Sprague-Dawley rats at 1, 2, 4, 8, and 16 wk after aortocaval fistula (shunt) was induced by the needle
technique. Three stages of cardiac hypertrophy due to volume
overload were recognized during the 16-wk period. Developing
hypertrophy occurred within the first 2 wk after aortocaval shunt was
induced and was characterized by a rapid increase of cardiac mass in
both left and right ventricles. Compensated hypertrophy occurred
between 2 and 8 wk after aortocaval shunt where normal or mild
depression in hemodynamic function was observed. Decompensated
hypertrophy or heart failure occurred between 8 and 16 wk after
aortocaval shunt and was characterized by circulatory congestion,
decreased in vivo and in vitro cardiac function, and a shift in myosin
heavy chain isozyme expression. However, the positive inotropic effect
of isoproterenol was augmented at all times during the 16-wk period.
Characterization of -adrenoceptor binding in failing hearts at 16 wk
revealed a significant increase in 1-receptor density,
whereas 2-receptor density was unchanged. Consistent
with this, basal adenylyl cyclase activity was significantly increased,
and both isoproterenol- and forskolin-stimulated adenylyl cyclase
activities were also increased. These results indicate that
upregulation of -adrenoceptor signal transduction is a unique feature of cardiac hypertrophy and failure induced by volume overload.
aortocaval fistula; -adrenergic mechanisms
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