Use of Tetanus to Investigate Myofibrillar Responsiveness to Ca2+ in Isolated Mouse Ventricular Myocytes.
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- Hongo Kenichi
- Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine
Bibliographic Information
- Other Title
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- Use of Tetanus to Investigate Myofibrillar Responsiveness to Ca〔2+〕 in Isolated Mouse Ventricular Myocytes
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Abstract
We used the relation between intracellular Ca2+ concentration ([Ca2+]i) and cell shortening during tetanus to evaluate the endogenous characteristics of Ca2+ responsiveness of myofibrils in mouse ventricular myocytes. Enzymatically isolated myocytes were loaded with fura-2 AM (4 μM for 10 min), and the fura-2 fluorescence ratio at 340 and 380 nm excitation wave length [F(340)/F(380)] and cell length were measured simultaneously. Following treatment with thapsigargin (0.2 μM) (an inhibitor of the Ca2+ pump of sarcoplasmic reticulum), myocytes were stimulated at 10 Hz for 10 s to produce a tetanic contraction and an instantaneous plot of the fluorescence ratio signal versus cell length (R-L trajectory) was constructed. An increase in the extracellular Ca2+ concentration ([Ca2+]o) from 0.5 to 2 mM extended the R-L trajectory without a substantial shift of the relation. The R-L trajectory was shifted rightward by the nonselective phosphodiesterase inhibitor, 3-isobutyl-1-methyl-xantine (IBMX, 200 μM) (desensitization of the myofibrils to Ca2+), and shifted leftward by the Ca2+ sensitizing thiadiazinone derivative, EMD-57033 (0.5 μM) (sensitization of the myofibrils to Ca2+). β-Adrenergic stimulant, isoproterenol (5 nM), also shifted the R-L trajectory to the right, suggesting that the membrane receptor could be preserved. These results suggest that the R-L trajectory is a useful method to estimate the myofibrillar responsiveness to Ca2+ in isolated mouse myocytes and can be applied to various mouse models of heart disease.<br>
Journal
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- The Japanese Journal of Physiology
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The Japanese Journal of Physiology 52 (1), 121-127, 2002
THE PHYSIOLOGICAL SOCIETY OF JAPAN
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Details 詳細情報について
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- CRID
- 1390282680020531712
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- NII Article ID
- 130004435826
- 10008296133
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- NII Book ID
- AA00691224
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- ISSN
- 18811396
- 0021521X
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- NDL BIB ID
- 6136030
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- PubMed
- 12047810
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- Text Lang
- en
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- Data Source
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- Abstract License Flag
- Disallowed