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Title: Occurrence of a tetrodotoxin-sensitive calcium current in rat ventricular myocytes after long-term myocardial infarction
Authors: Alvarez, JL ×
Salinas-Stefanon, E
Orta, G
Ferrer, T
Talavera PĂ©rez, Karel
Galan, L
Vassort, G #
Issue Date: Sep-2004
Publisher: Elsevier science bv
Series Title: Cardiovascular Research vol:63 issue:4 pages:653-661
Abstract: 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 a-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 I-Ca(TTX) current previously reported. I-Ca(TTX)-like current was critically dependent on extracellular Na+ and was reduced by micromolar Na+ concentrations. Neither in normal rat cardiornyocytes 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 I-Ca(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. (C) 2004 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
URI: 
ISSN: 0008-6363
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Laboratory of Ion Channel Research
× corresponding author
# (joint) last author

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