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Europace Advance Access originally published online on June 19, 2007
Europace 2007 9(8):571-577; doi:10.1093/europace/eum121
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

BASIC SCIENCE

Effects of heart failure on brain-type Na+ channels in rabbit ventricular myocytes

Arie O. Verkerk1, Antoni C.G. van Ginneken1, Toon A.B. van Veen2 and Hanno L. Tan1,3,*

1 Heart Failure Research Center, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; 2 Department of Medical Physiology, University Medical Center Utrecht, Utrecht, The Netherlands; 3 Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

Aims Brain-type {alpha}-subunit isoforms of the Na+ channel are present in various cardiac tissue types and may control pacemaker activity and excitation–contraction coupling. Heart failure (HF) alters pacemaker activity and excitation–contraction coupling. Here, we studied whether HF alters brain-type Na+ channel properties.

Methods and results HF was induced in rabbits by volume/pressure overload. Na+ currents of ventricular myocytes were recorded in the cell-attached mode of the patch-clamp technique using macropatches. Macropatch recordings were conducted from the middle portions of myocytes or from intercalated disc regions between cell pairs. Both areas exhibited a fast activating and inactivating current, 8.5 times larger in intercalated disc regions. Tetrodotoxin (TTX) (50 nM) did not block currents in the intercalated disc regions, but did block in the middle portions, indicating that the latter currents were TTX-sensitive brain-type Na+ currents. Macropatch recordings from these regions were used to study the effects of HF on brain-type Na+ current. Neither current density nor gating properties (activation, inactivation, recovery from inactivation, slow inactivation) differed between CTR and HF.

Conclusion The density and gating properties of brain-type Na+ current are not altered in our HF model. In the volume/pressure-overload rabbit model of HF, the role of brain-type Na+ current in HF-induced changes in excitation–contraction coupling is limited.

Key Words: Heart failure, Sodium current, Excitation–contraction coupling, Pacemaker activity

* Corresponding author. Tel: +31 20 5663265; fax: +31 20 6975458. E-mail address: h.l.tan{at}amc.uva.nl

Manuscript submitted 11 January 2007. Accepted after revision 16 May 2007.


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S. Petitprez and H. Abriel
Effects of heart failure on brain-type Na+ channels in rabbit ventricular myocytes
Europace, February 1, 2008; 10(2): 257 - 257.
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A. O. Verkerk, A. C.G. van Ginneken, T. A.B. van Veen, and H. L. Tan
Effects of heart failure on brain-type Na+ channels in rabbit ventricular myocytes: Reply
Europace, February 1, 2008; 10(2): 257 - 258.
[Full Text] [PDF]


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