Abstract
As is well known, force generation and contractility of the heart may be controlled by calcium by way of regulating crossbridge attachment and the transition of attaching crossbridges into a force-generating state. These calcium activation processes do not occur in an all-or-none manner, but may be graded e.g. by altering the degree of calcium occupancy of troponin C (e.g. Pan and Solaro, 1987). Calcium occupancy depends on the free calcium concentration in the myoplasm in the range of 0.1 to 10 μM, but also, of course, on the calcium affinity of troponin C. Thus, at an intermediate cytosolic Ca2+ concentration allowing force to reach half maximum activation, any increase in calcium affinity would increase calcium occupancy and hence force and contractility. Thus, a lower Ca2+ concentration (or for that matter a higher pCa50 value) would then be required to reach half maximum activation under these conditions. This we refer to as Ca2+ sensitization of the myofilaments. The term calcium sensitivity modulation then is taken to mean a change in the pCa50 value, i.e. in the level of ionised calcium required for 50% activation of the myofilament activity normalized to the maximum contractile activity at saturating levels of calcium.
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Rüegg, J.C. (2003). Pharmacological Calcium Sensitivity Modulation of Cardiac Myofilaments. In: Sugi, H. (eds) Molecular and Cellular Aspects of Muscle Contraction. Advances in Experimental Medicine and Biology, vol 538. Springer, Boston, MA. https://doi.org/10.1007/978-1-4419-9029-7_37
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DOI: https://doi.org/10.1007/978-1-4419-9029-7_37
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