Remodeling excitation-contraction coupling of hypertrophied ventricular myocytes is dependent on T-type calcium channels expression

Satoshi Takebayashi, Yulong Li, Toshihiko Kaku, Shuichiro Inagaki, Yutaka Hashimoto, Kazuhiro Kimura, Shinji Miyamoto, Tetsuo Hadama, Katsushige Ono

Research output: Contribution to journalArticle

29 Scopus citations

Abstract

We utilized Wistar rats with monocrotaline (MCT)-induced right ventricular hypertrophy (RVH) in order to evaluate the T-type Ca2+ channel current (ICaT) for myocardial contraction. RT-PCR provides that mRNA for T-type Ca2+ channel α1-subunits in hypertrophied myocytes was significantly higher than those in control rats (α1G; 264 ± 36%, α1H; 191 ± 34%; P < 0.05). By whole-cell patch-clamp study, ICaT was recorded only in hypertrophied myocytes but not in control myocytes. The application of 50 nmol/L nifedipine reduced the twitch tension of the right ventricles equally in the control and RVH rats. On the other hand, 0.5 μmol/L mibefradil, a T-type Ca2+ channel blocker, strongly inhibited the twitch tension of the RVH muscle (control 6.4 ± 0.8% vs. RVH 20.0 ± 2.3% at 5 Hz; P < 0.01). In conclusion, our results indicate the functional expression of T-type Ca2+ channels in the hypertrophied heart and their contribution to the remodeling of excitation-contraction coupling in the cardiac myocyte.

Original languageEnglish (US)
Pages (from-to)766-773
Number of pages8
JournalBiochemical and Biophysical Research Communications
Volume345
Issue number2
DOIs
StatePublished - Jun 30 2006

Keywords

  • E-C coupling
  • Hypertrophy
  • Remodeling
  • T-type Ca channels

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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