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Départements de 1 Pharmacologie et de 5 Biochimie, Faculté de Médecine, Université de Montréal, Québec H3C 3J7; 2 Centre de Recherche, Hôpital du Sacré-Coeur de Montréal, Montréal, Québec H4J 1C5; and 3 Department of Obstetrics and Gynaecology and 4 Department of Physiology and Biophysics, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia B3H 4B7, Canada
To corroborate
alterations in the functional responses to 
-adrenergic receptor
(-AR) stimulation with changes in -AR signaling in
failing cardiomyocytes, contractile and L-type Ca2+ current
responses to isoproterenol along with stimulated cAMP generation were
compared among cardiomyocytes isolated from canines with
tachycardia-induced heart failure or healthy hearts. The magnitude of
shortening of failing cardiomyocytes was significantly depressed (by
22 ± 4.4%) under basal conditions, and the maximal response to
isoproterenol was significantly reduced (by 45 ± 18%). Similar
results were obtained when the responses in the rate of contraction and
rate of relaxation to isoproterenol were considered. The L-type
Ca2+ current amplitude measured in failing cardiomyocytes
under basal conditions was unchanged, but the responses to
isoproterenol were significantly reduced compared with healthy cells.
Isoproterenol-stimulated cAMP generation was similar in sarcolemmal
membranes derived from the homogenates of failing (45 ± 6.8) and
healthy cardiomyocytes (52 ± 8.5 pmol cAMP · mg
protein
1 · min1). However,
stimulated cAMP generation was found to be significantly reduced when
the membranes were derived from the homogenates of whole tissue
(failing: 67 ± 8.1 vs. healthy: 140 ± 27.8 pmol
cAMP · mg protein1 · min1).
Total -AR density was not reduced in membranes derived from either
whole tissue or isolated cardiomyocyte homogenates, but the
1/2 ratio was significantly reduced in
the former (failing: 45/55 vs. healthy: 72/28) without being altered in
the latter (failing: 72/28, healthy: 77/23). We thus conclude that, in
tachycardia-induced heart failure, reduction in the functional
responses of isolated cardiomyocytes to -AR stimulation may be
attributed to alterations in the excitation-contraction machinery
rather than to limitation of cAMP generation.
-adrenergic receptor; heart failure; cardiomyocytes; adenylyl
cyclase; contraction
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