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Cardiovascular Research 2004 63(4):653-661; doi:10.1016/j.cardiores.2004.05.010
© 2004 by European Society of Cardiology
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Copyright © 2004, European Society of Cardiology

Occurrence of a tetrodotoxin-sensitive calcium current in rat ventricular myocytes after long-term myocardial infarction

Julio L Alvareza,b, Eduardo Salinas-Stefanonc, Gerardo Ortac, Tania Ferrerb, Karel Talaverab, Loipa Galánb and Guy Vassort*,a

aINSERM U-390, Physiopathologie Cardiovasculaire, CHU Arnaud de Villeneuve, 371 Avenue du Doyen Gaston Giraud, F-34295 Montpellier Cedex 5, France
bInstituto de Cardiología y Cirugía Cardiovascular, Havana, Cuba
cInstituto de Fisiología, Universidad Autónoma de Puebla, Puebla, Mexico

* Corresponding author. Tel.: +33-4-67-41-52-41; fax: +33-4-67-41-52-42. Email address: vassort{at}montp.inserm.fr

Objective: To determine the characteristics of a TTX-sensitive Ca2+ current that occurred only following remodelling after myocardial infarction in Wistar rat. Methods: Using the whole-cell patch-clamp technique, we studied ionic inward current in myocytes isolated from four different ventricular regions of control Wistar rat hearts, or from hearts 4 to 6 months after ligation of the left coronary artery. Inward current characteristics were also analysed in Xenopus laevis oocytes that heterologously expressed the human sodium channel {alpha}-subunit Nav1.5. The effects of oxidative stress by hydrogen peroxide or tert-butyl-hydroxyperoxide as well as those of PKA-dependent phosphorylation, which partly mimic the pathological conditions, were investigated on control cardiomyocytes and Nav1.5-expressing oocytes. Results: In Na-free solution, a low-threshold, tetrodotoxin-sensitive inward current was found in 20 out of 78 cells isolated from 16 post-myocardial infarcted (PMI) cardiomyocytes but not in cardiomyocytes from young and sham rat hearts. This current exhibited kinetics and pharmacological properties similar to the ICa(TTX) current previously reported. ICa(TTX)-like current was critically dependent on extracellular Na+ and was reduced by micromolar Na+ concentrations. Neither in normal rat cardiomyocytes nor in Nav1.5-expressing oocytes could a ICa(TTX)-like current be elicited in Na+-free extracellular solution, even after oxidative stress or PKA-dependent phosphorylation. Conclusions: Our data suggest that ICa(TTX)-like current in PMI myocytes does not arise from classical Na+ channels modified by oxidative stress or PKA phosphorylation and most probably represents a different Na+ channel type re-expressed in some cells after remodelling.

KEYWORDS Arrhythmia; Heart failure; Na-channel; Oxidative phosphorylation; Remodelling

Time for primary review 25 days


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