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Department of Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205
Length-dependent steady-state and dynamic
responses of five models of isometric force generation in cardiac
myofilaments were compared with similar experimental data from the
literature. The models were constructed by assuming different subsets
of three putative cooperative mechanisms. Cooperative
mechanism 1 holds that cross-bridge binding increases
the affinity of troponin for Ca2+.
In the models, cooperative mechanism 1 can produce steep force-Ca2+
(F-Ca) relations, but apparent cooperativity is highest at midlevel Ca2+ concentrations. During
twitches, cooperative mechanism 1 has the effect of increasing latency to peak as the magnitude of force increases, an effect not seen experimentally.
Cooperative mechanism 2 holds that the
binding of a cross bridge increases the rate of formation of
neighboring cross bridges and that multiple cross bridges can maintain
activation of the thin filament in the absence of
Ca2+. Only
cooperative mechanism 2 can produce
sarcomere length (SL)-dependent prolongation of twitches, but this
mechanism has little effect on steady-state F-Ca relations.
Cooperativity mechanism 3 is designed to simulate end-to-end interactions between adjacent troponin and
tropomyosin. This mechanism can produce steep F-Ca relations with
appropriate SL-dependent changes in
Ca2+ sensitivity. With the
assumption that tropomyosin shifting is faster than cross-bridge
cycling, cooperative mechanism 3 produces twitches where latency to peak is independent of the magnitude of force, as seen experimentally.
myofilaments; modeling; twitches; force-calcium relations; isometric relaxation
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