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-adrenoceptor density in pacing-induced heart failure
Cardiology Unit, Department of Medicine, Department of Neurobiology and Anatomy, University of Rochester Medical Center, Rochester, New York 14642
Congestive heart failure is associated with cardiac
adrenergic nerve terminal changes and 
-adrenoceptor density
downregulation. To study the temporal sequence of these changes, we
performed studies in rabbits at 2, 4, and 8 wk of cardiac pacing (360 beats/min) and at 1, 2, and 4 wk after cessation of pacing. Rapid
pacing produced left ventricular (LV) dysfunction and an increase in plasma norepinephrine (NE) in 1-2 wk. At week 2, NE uptake
activity, NE uptake-1 density, and adenylyl cyclase responses to
isoproterenol, 5'-guanylyl imidodiphosphate
[Gpp(NH)p], and forskolin reduced. However, immunostained
tyrosine hydroxylase profile, -adrenoceptor density, and NE
histofluorescence did not reduce until 4-8 wk of pacing. After
cessation of cardiac pacing, LV function normalized quickly, followed
by return of tyrosine hydroxylase and NE profiles in 1 wk and adenylyl
cyclase responses to agonists and NE uptake activity in 2 wk.
Myocardial -adrenoceptor density returned to normal by 4 wk after
cessation of pacing. Our results suggest that there is no permanent
structural neuronal damage in the myocardium within the first 8 wk of
rapid cardiac pacing. Abnormal myocardial NE reuptake mechanism may
play an important pathophysiological role in heart failure.
norepinephrine; norepinephrine reuptake; adrenergic nerve terminals; pacing-induced cardiomyopathy
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