Literature DB >> 15306221

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

Julio L Alvarez1, Eduardo Salinas-Stefanon, Gerardo Orta, Tania Ferrer, Karel Talavera, Loipa Galán, Guy Vassort.   

Abstract

OBJECTIVE: To determine the characteristics of a TTX-sensitive Ca(2+) 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 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 cardiomyocytes nor in Nav1.5-expressing oocytes could a I(Ca(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.

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Year:  2004        PMID: 15306221     DOI: 10.1016/j.cardiores.2004.05.010

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  5 in total

1.  Tetrodotoxin blocks L-type Ca2+ channels in canine ventricular cardiomyocytes.

Authors:  Bence Hegyi; László Bárándi; István Komáromi; Ferenc Papp; Balázs Horváth; János Magyar; Tamás Bányász; Zoltán Krasznai; Norbert Szentandrássy; Péter P Nánási
Journal:  Pflugers Arch       Date:  2012-05-22       Impact factor: 3.657

2.  Tetrodotoxin-sensitive Ca2+ Currents, but No T-type Currents in Normal, Hypertrophied, and Failing Mouse Cardiomyocytes.

Authors:  Ilona Bodi; Hiroyuki Nakayama; Arnold Schwartz
Journal:  J Cardiovasc Pharmacol       Date:  2016-12       Impact factor: 3.105

3.  Differential interactions of Na+ channel toxins with T-type Ca2+ channels.

Authors:  Hui Sun; Diego Varela; Denis Chartier; Peter C Ruben; Stanley Nattel; Gerald W Zamponi; Normand Leblanc
Journal:  J Gen Physiol       Date:  2008-07       Impact factor: 4.086

4.  Tetrodotoxin blockade on canine cardiac L-type Ca²⁺ channels depends on pH and redox potential.

Authors:  Bence Hegyi; István Komáromi; Kornél Kistamás; Ferenc Ruzsnavszky; Krisztina Váczi; Balázs Horváth; János Magyar; Tamás Bányász; Péter P Nánási; Norbert Szentandrássy
Journal:  Mar Drugs       Date:  2013-06-14       Impact factor: 5.118

5.  Regional differences in the expression of tetrodotoxin-sensitive inward Ca2+ and outward Cs+/K+ currents in mouse and human ventricles.

Authors:  Wei Wang; Rebecca L Mellor; Jeanne M Nerbonne; C William Balke
Journal:  Channels (Austin)       Date:  2019-12       Impact factor: 2.581

  5 in total

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