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 language | English (US) |
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Pages (from-to) | 766-773 |
Number of pages | 8 |
Journal | Biochemical and Biophysical Research Communications |
Volume | 345 |
Issue number | 2 |
DOIs | |
State | Published - Jun 30 2006 |
Keywords
- E-C coupling
- Hypertrophy
- Remodeling
- T-type Ca channels
ASJC Scopus subject areas
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology