Development of Excitation-Contraction Coupling in Cardiomyocytes
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- Tohse Noritsugu
- Department of Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine
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- Seki Sumihiko
- Department of Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine
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- Kobayashi Takeshi
- Department of Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine
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- Tsutsuura Masaaki
- Department of Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine
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- Nagashima Masato
- Department of Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine
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- Yamada Yoichi
- Department of Cellular Physiology and Signal Transduction, Sapporo Medical University School of Medicine
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説明
The excitation-contraction (E-C) coupling system during the development of heart can be investigated because of marked progression in electrophysiology and microfluorescence studies. During the developmental period, Ca2+ influx mediating the E-C coupling is mainly through the L-type Ca2+ channels. In the fetal period, T-type Ca2+ channels and the reverse mode of the Na-Ca exchange system also contribute to Ca2+ influx. These contributions probably reduce gradually until adulthood. The contraction of fetal cardiomyocytes has been thought to depend mainly on the Ca2+ influx. However, recent studies reveal that immature sarcoplasmic reticulum (SR) already works in the early fetal period. Ca2+ spark, a local and unitary movement of Ca2+, can be observed in adult cardiomyocytes by the use of a confocal microscope. On the other hand, no Ca2+ spark is observed in fetal cardiomyocytes. The frequency of Ca2+-spark evocation increases during the postnatal period. Therefore a close distance between the L-type Ca2+ channel and the SR Ca2+-release channel is essential to the establishment of the Ca2+ spark.<br>
収録刊行物
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- The Japanese Journal of Physiology
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The Japanese Journal of Physiology 54 (1), 1-6, 2004
一般社団法人 日本生理学会
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詳細情報 詳細情報について
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- CRID
- 1390282680020079360
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- NII論文ID
- 130004435884
- 80016562003
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- NII書誌ID
- AA00691224
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- COI
- 1:STN:280:DC%2BD2c7kvVyntQ%3D%3D
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- ISSN
- 18811396
- 0021521X
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- NDL書誌ID
- 6893264
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- PubMed
- 15040842
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可