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Cardiovascular Research 2000 45(3):713-719; doi:10.1016/S0008-6363(99)00370-3
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Adrenergic regulation of myocardial apoptosis

Krishna Singh, Catherine Communal, Douglas B. Sawyer and Wilson S. Colucci*

Myocardial Biology Unit and Cardiovascular Division, Boston University Medical Center, Boston Veterans Affairs Medical Center and Boston University School of Medicine, 88 East Newton Street, Boston, MA 02118, USA

* Corresponding author. Tel.: +1-617-638-8706; fax: +1-617-638-8712 wilson.colucci{at}bmc.org

Increased sympathetic nerve activity to the myocardium is a central feature in patients with heart failure. Norepinephrine, the primary transmitter of the sympathetic nervous system, signals via binding to {alpha}- and β-adrenergic receptors (AR) that are coupled to G-proteins. Pharmacologic studies of cardiac myocytes in vitro demonstrate that β-AR can stimulate apoptosis. Likewise, in transgenic mice overexpression of β1-AR or G{alpha}s is associated with myocyte apoptosis and the development of dilated cardiomyopathy. Whereas β1-AR stimulate apoptosis in vitro and in vivo, β2-AR may either stimulate or inhibit apoptosis and myocardial failure depending on the level of expression. Receptors coupling to Gi and Gq may also be able to mediate or modulate apoptosis and the development of myocardial failure, suggesting the potential for interactions between the β-AR system and numerous remodeling stimuli that act through Gi or Gq signaling pathways. It appears likely that the mitogen-activated protein kinase superfamily plays a key role in mediating the actions of adrenergic pathways on myocyte apoptosis. These observations suggest that the adrenergic nervous system plays an important role in the regulation of myocyte apoptosis, and may thus contribute to the development of myocardial failure.

KEYWORDS Adrenergic (ant)agonists; Apoptosis; Autonomic nervous system; G-proteins; Heart failure; Receptors; Signal transduction


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