Abstract:
:To explain observed differences in the activation dependence of force redevelopment kinetics between cardiac and skeletal muscle, two numerical models of contractile regulation by Ca2+ were investigated. Ca2+ binding and force production were each modelled as two-state processes with forward and reverse rate constants taken from the literature. The first model incorporates four possible thin-filament states. In the second model Ca2+ is assumed not to dissociate from a thin-filament unit in the force-generating state, resulting in three states. The four-state model can account for the activation dependence of the rate constant of tension redevelopment (ktr) seen in skeletal muscle, without requiring that Ca2+ directly modulates the kinetics of any step in the cross-bridge cycle. Using identical kinetic parameters, the three-state model shows no activation dependence of ktr, consistent with our results in cardiac muscle. Following a step increase in [Ca2+], the rate of rise in tension (as described by the rate constant kCa) varies with the final [Ca2+] for both models, consistent with experimental results from skeletal and cardiac muscle. These numerical models demonstrate that experimental measurements thought to reveal changes in kinetic parameters may simply reflect coupling between the two kinetic processes of Ca2+ binding and force generation. Furthermore, the models present possible differences in the Ca2+ activation scheme between cardiac and skeletal muscle which can account for the contrasting activation dependencies of force redevelopment kinetics.
journal_name
J Muscle Res Cell Motiljournal_title
Journal of muscle research and cell motilityauthors
Hancock WO,Huntsman LL,Gordon AMdoi
10.1023/a:1018635907091subject
Has Abstractpub_date
1997-12-01 00:00:00pages
671-81issue
6eissn
0142-4319issn
1573-2657journal_volume
18pub_type
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journal_title:Journal of muscle research and cell motility
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journal_title:Journal of muscle research and cell motility
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1007/BF01578427
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1023/a:1024830132118
更新日期:2003-01-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章,评审
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更新日期:2002-01-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1023/a:1005455505056
更新日期:1998-10-01 00:00:00
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journal_title:Journal of muscle research and cell motility
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更新日期:2009-01-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1007/BF01739856
更新日期:1989-02-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1007/s10974-008-9145-x
更新日期:2008-01-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1023/a:1014543507149
更新日期:2001-01-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1007/BF00114505
更新日期:1995-08-01 00:00:00
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journal_title:Journal of muscle research and cell motility
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doi:10.1007/s10974-005-9044-3
更新日期:2006-01-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1007/BF00123833
更新日期:1994-02-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1023/b:jure.0000009896.78385.16
更新日期:2003-01-01 00:00:00
abstract::Several mutations in the beta-myosin heavy chain gene cause hypertrophic cardiomyopathy. This study investigates (1) the in vitro velocities of translocation of fluorescently-labelled actin by beta-myosin purified from soleus muscle of 30 hypertrophic cardiomyopathy patients with seven distinct beta-myosin heavy chain...
journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1023/a:1018613907574
更新日期:1997-06-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章,评审
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journal_title:Journal of muscle research and cell motility
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章,评审
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1007/BF00122120
更新日期:1994-08-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
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更新日期:1988-12-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
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更新日期:1981-03-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
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更新日期:1992-04-01 00:00:00
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journal_title:Journal of muscle research and cell motility
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更新日期:2004-01-01 00:00:00
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章,评审
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journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1007/BF00121071
更新日期:1994-12-01 00:00:00
abstract::Our current understanding of the structure of the thin filaments of muscle and the molecular mechanism by which thin filaments regulate muscle contraction are reviewed and discussed. We focus, in particular, on the crucial role played by Jean Hanson in these studies and on later contributions from those whose work she...
journal_title:Journal of muscle research and cell motility
pub_type: 传,历史文章,杂志文章,评审
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更新日期:2004-01-01 00:00:00
abstract::The change in orientation of myosin crossbridges in contracting muscle during sudden length changes was examined by fluorescence polarization. This study used a fluorescent ATP analogue, 1,N6-etheno-2-aza-ATP(epsilon-2-aza-ATP) as a probe. Its fluorescence is considerably enhanced upon binding with myosin and is depen...
journal_title:Journal of muscle research and cell motility
pub_type: 杂志文章
doi:10.1007/BF00712310
更新日期:1985-02-01 00:00:00