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1B-adrenergic receptor
induces left ventricular dysfunction in the absence of
hypertrophy
Departments of 1 Pharmacology and Cell Biophysics, 2 Molecular and Cellular Physiology, 3 Internal Medicine, and 4 Pathology, University of Cincinnati, Cincinnati, Ohio 45267; and 5 Department of Medicine, University of Montreal, and Montreal Heart Institute, Montreal, Quebec, Canada H1T 1C8
The stimulation of cardiac
1-adrenergic receptors (AR)
modulates the heart's inotropic response and plays a role in the
induction of cardiomyocyte hypertrophy. We have analyzed transgenic
mouse lines overexpressing a wild-type
1B-AR specifically in the
heart. Basal level systolic and diastolic left ventricular (LV)
contractile function was depressed both in the anesthetized
closed-chest mouse and the perfused working-heart preparation.
Intrinsic LV function was further characterized under controlled
preload and afterload conditions using the perfusion model. Contractile
parameters were restored by chronic treatment with the -AR
antagonist prazosin. In ventricular function curves, the load-dependent
force increases (length-tension effects) remained intact, although the
transgenic curve was shifted to lower levels. The basal level
contractile deficits were paralleled by a decrease in calcium
transients in isolated LV cardiomyocytes. LV function comparable to
controls was restored by isoproterenol stimulation. The physiological
changes occurred in the absence of cardiomyocyte hypertrophy. This
transgenic model will be useful for studying the potential role of
1-AR in cardiac contractility
and hypertrophy.
heart; myocardial contractility; muscle; transgenic mouse
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