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Am J Physiol Heart Circ Physiol (July 26, 2002). doi:10.1152/ajpheart.01063.2001
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Articles in PresS, published online ahead of print July 26, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01063.2001
Submitted on December 4, 2001
Accepted on July 12, 2002

Abnormal Cardiac Function Associated with Sympathetic Nervous System Hyperactivity in Mice

Patricia C Brum1, Jon Kosek1, Andrew Patterson1, Daniel Bernstein1, and Brian K Kobilka1*

1 Molecular and Cellular Physiology, Stanford University, Stanford, CA, USA

* To whom correspondence should be addressed. E-mail: kobilka{at}stanford.edu.

{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 months of age. These knockout mice have increased mortality, reduced exercise capacity, decreased peak oxygen uptake, and decreased contractility relative to wild type controls. Moreover, we observe significant abnormalities in the ultrastructure of cardiac myocytes from {alpha}2A/{alpha}2C adrenoceptor 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 hear failure.




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