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pubmed-article:8676541pubmed:abstractTextA change in muscle length significantly alters the developed tension in mammalian cardiac muscle compared to that in skeletal muscle fibers. The intracellular mechanisms related to the length-dependent change in developed tension have been studied using Ca2+ indicators in intact preparations; a cross-bridge-dependent change in the affinity of troponin-C for Ca2+ is a possible mechanism. This hypothesis is further supported by the measurement of Ca2+ bound to troponin-C in skinned preparations. The molecular mechanism of the cross-bridge-dependent change in the affinity of troponin-C for Ca2+ is not fully understood although the studies which employ the substitution of troponin-C in skinned preparations, transgenic animals and in an animal model with heart disease have been performed. We reviewed the current studies by analyzing the intracellular mechanism responsible for the length-dependent change in tension development in mammalian cardiac muscle.lld:pubmed
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pubmed-article:8676541pubmed:authorpubmed-author:KuriharaSSlld:pubmed
pubmed-article:8676541pubmed:authorpubmed-author:KomukaiKKlld:pubmed
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pubmed-article:8676541pubmed:volume37lld:pubmed
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pubmed-article:8676541pubmed:pagination143-52lld:pubmed
pubmed-article:8676541pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:8676541pubmed:year1996lld:pubmed
pubmed-article:8676541pubmed:articleTitleCross-bridge-dependent changes in the intracellular Ca2+ concentration in mammalian cardiac muscles.lld:pubmed
pubmed-article:8676541pubmed:affiliationDepartment of Physiology, Jikei University School of Medicine, Tokyo, Japan.lld:pubmed
pubmed-article:8676541pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8676541pubmed:publicationTypeReviewlld:pubmed
pubmed-article:8676541pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed