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Cardiovascular Research 2003 59(2):262-265; doi:10.1016/S0008-6363(03)00477-2
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Negative inotropy starts with the β3-adrenoceptor

Enn K. Seppet*

Department of Pathophysiology, Faculty of Medicine, University of Tartu, 19 Ravila Street, 50411 Tartu, Estonia

* Tel.: +372-7-374-371; fax: +372-7-374-372. enn@ut.ee

Received 3 June 2003; revised 6 June 2003; accepted 6 June 2003

The first 150 words of the full text of this article appear below.

See article by Tavernier et al. [1] (pages 288–296) in this issue.

In this issue of Cardiovascular Research, Tavernier et al. describe the effects of β3-adrenergic stimulation on cardiac contractility in mice overexpressing the human β3-adrenoceptor (β3-AR) [1]. This study is a logical sequel to preceding investigations by the same research group that also provided the first evidence of the existence and functional role of this AR subtype in the human heart [2]. That time it was found that in contrast to the classical effects of β1-/β2-adrenergic system—positive inotropy and lusitropy—activation of β3-AR results in negative inotropy via a Gi protein-dependent pathway. Further studies revealed that β3-AR stimulation attenuates cardiac contractility through increased nitric oxide (NO) production and intracellular cGMP [3,4].

To further explore the properties and role of the β3-adrenergic system, Tavernier et al. [1] generated transgenic . . . [Full Text of this Article]


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