ABSTRACT
In this chapter, we focus on regulation of the intensity of activity and dynamics of the myocardium by control mechanisms operating at the level of sarcomeric proteins. This mode of regulation includes mechanisms that control cardiac function downstream of alterations in membrane-related Ca2+ release, transport, and exchange mechanisms. Experimental evidence for this type of regulation is largely couched in terms of the relation between Ca2+ and steady-state tension developed by either single or bundled cells in which the membrane has been removed or made permeable by detergent treatment (skinned or peeled fibers). An altered Ca2+ sensitivity of the myofilaments is reflected in a shift of the half-maximally activating Ca2+ concentration, the maximum tension, or the steepness of the relation between Ca2+ and force. Another perhaps more relevant measure of Ca2+ sensitivity is the determination of the temporal relation between Ca2+ and force or shortening. In this case, changes in mechanical activity independent of changes in the Ca2+ provide strong evidence for an altered myofilament response to Ca2+.
