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Cardiovascular Research 2002 56(3):353-356; doi:10.1016/S0008-6363(02)00706-X
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

β3-Adrenoceptors in the heart

Chantal E. Conratha and Tobias Opthofb,*

aDepartment of Cardiology, University Medical Center, Utrecht, The Netherlands
bDepartment of Medical Physiology, University Medical Center, P.O. Box 85060, 3508 AB Utrecht, The Netherlands

t.opthof@med.uu.nl

* Corresponding author. Tel.: +31-30-253-8900; fax: +31-30-253-9036.

accepted 1 October 2002

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

See article by Bosch et al. [4] (pages 393–403) in this issue.

The existence of β3-adrenoceptors has been demonstrated in the human ventricle [1]. The therapeutic indications for β3-adrenoceptor agonists are obesity and obesity linked diabetes [1]. Because negative inotropy has been reported in response to β3-adrenoceptor stimulation in human ventricle [1,2] as well as in guinea pig ventricle [3], a study of effects on cardiac membrane currents is highly relevant.

In this issue of Cardiovascular Research Bosch and colleagues [4] describe the effect of β3-adrenoceptor stimulation on the membrane current IKs (slow component of the delayed rectifier current underlying repolarization) as well as on action potential duration in guinea pig ventricular myocytes. β3-Adrenoceptor stimulation was produced in two ways: either by isoproterenol or noradrenaline in combination with specific blockers of the β1-(atenolol) plus the β2-adrenoceptors (ICI 118,551) or by . . . [Full Text of this Article]


   1 β3-Adrenoceptor stimulation and membrane currents
 

   2 β3-Adrenoceptor stimulation and action potential duration
 

   3 Evolutionary and teleological considerations
 

   4 Could β3-adrenoceptor antagonists be useful in heart failure?
 

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