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Am J Physiol Heart Circ Physiol 283: H1838-H1845, 2002. First published July 26, 2002; doi:10.1152/ajpheart.01063.2001
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Vol. 283, Issue 5, H1838-H1845, November 2002

Abnormal cardiac function associated with sympathetic nervous system hyperactivity in mice

Patricia C. Brum2, Jon Kosek1, Andrew Patterson3, Daniel Bernstein4, and Brian Kobilka2,5

1 Department of Pathology, Veterans Administration Medical Center, Palo Alto 94305; and 2 Departments of Medicine and Molecular and Cellular Physiology, 3 Department of Anesthesia, 4 Division of Cardiology, Department of Pediatrics, and 5 Howard Hughes Medical Institute, Stanford University, Stanford, California 94305

alpha 2A-Adrenergic receptors (ARs) in the midbrain regulate sympathetic nervous system activity, and both alpha 2A-ARs and alpha 2C-ARs regulate catecholamine release from sympathetic nerve terminals in cardiac tissue. Disruption of both alpha 2A- and alpha 2C-ARs in mice leads to chronically elevated sympathetic tone and decreased cardiac function by 4 mo of age. These knockout mice have increased mortality, reduced exercise capacity, decreased peak oxygen uptake, and decreased cardiac contractility relative to wild-type controls. Moreover, we observed significant abnormalities in the ultrastructure of cardiac myocytes from alpha 2A/alpha 2C-AR knockout mice by electron microscopy. Our results demonstrate that chronic elevation of sympathetic tone can lead to abnormal cardiac function in the absence of prior myocardial injury or genetically induced alterations in myocardial structural or functional proteins. These mice provide a physiologically relevant animal model for investigating the role of the sympathetic nervous system in the development and progression of heart failure.

alpha 2-adrenergic receptor; knockout mice; heart failure


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