2010 Fiscal Year Final Research Report
Elucidation of the Frank-Starling mechanism of the heart by thin filament reconstitution
| Project/Area Number |
20500368
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Neurophysiology and muscle physiology
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
FUKUDA Norio Jikei University School of Medicine, 医学部, 准教授 (30301534)
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| Co-Investigator(Kenkyū-buntansha) |
KURIHARA Satoshi 東京慈恵会医科大学, 医学部, 教授 (90057026)
OHTSUKI Iwao 東京慈恵会医科大学, 医学部, 教授 (70009992)
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| Co-Investigator(Renkei-kenkyūsha) |
ISHIWATA Shin'ichi 東京慈恵会医科大学 (10130866)
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| Project Period (FY) |
2008 – 2010
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| Keywords | 生理学 / 生物物理 / 細胞・組織 / 生物・生体工学 / 生体分子 |
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| Research Abstract |
Cardiac sarcomeres produce greater active force in response to stretch, forming the basis of the Frank-Starling mechanism of the heart. The purpose of this study was to provide the systematic understanding of length-dependent activation, by investigating experimentally and mathematically how the thin filament "on-off" switching mechanism is involved in the regulation. Our experimental analyses revealed that the magnitude of length-dependent activation was inversely correlated with thin filament cooperative activation. These results were quantitatively simulated by a model that incorporates the Ca^<2+>-dependent "on-off" switching of the thin filament state and interfilament lattice spacing modulation. These findings demonstrate that the Frank-Starling relation is regulated by thin filament cooperative activation.
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