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Titlebook: Excitation-Contraction Coupling and Cardiac Contractile Force; Donald M. Bers Book 1993 Springer Science+Business Media Dordrecht 1993 Cal

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Cardiac Inotropy and Ca Overload,ress strategic sites for induction of cardiac inotropy. These discussions may help to bring some of the characteristics of specific cellular systems discussed in preceding chapters into a more integrative picture of cellular Ca regulation.
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Myofilaments: The End Effector of E-C Coupling,TP) into mechanical force or shortening. Under physiological conditions, skeletal muscle contractile force can be varied by summation of contractions, tetanus and recruitment of additional fibers. Cardiac muscle, on the other hand, functions as a syncytium such that each cell contracts at every beat
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Possible Sources and Sinks of Activator Calcium,uch Ca is required. The Ca binding of the cardiac myofilaments and of homogenized ventricular muscle were measured by Solaro .. (1974) and Pierce .. (1985), respectively. Fabiato (1983) also calculated the buffering capacity based on many estimates of the Ca buffering site concentrations and affinit
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Ca Influx Via Sarcolemmal Ca Channels,haracterized as “slow inward current” or I., since several tens of msec were required for peak current to be achieved (e.g. Rougier .., 1969; Mascher & Peper, 1969; Beeler & Reuter, 1970; Ochi, 1970). Since the advent of the patch-clamp technique it has become clear that Ca current (I.) can reach a
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Na/Ca Exchange and the Sarcolemmal Ca-Pump,e Capump was first reported in erythrocytes (Schatzmann, 1966) and has since been demonstrated in many other cells (Schatzmann, 1982, 1989). The red cell plasma membrane Ca-pump has been most extensively characterized and appears closely related to that in other tissues. The purified protein is 138
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