Abstract
The basis of the Frank-Starling mechanism of the heart is the intrinsic ability of myocardial fibers to produce greater active force in response to stretch (i.e., length-dependent activation). We have reported that titin (connectin)-based passive force plays an important role in this phenomenon (e.g., Fukuda et al., Circulation 2001; J. Physiol. 2003). In the present study, we investigated whether or not length-dependent activation is regulated at the thin filament level by using a quasi-complete troponin exchange technique.
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