Abstract
Cardiac contraction is regulated by a number of Ca2+-mediated processes. Here we consider the effects of modification imposed on the Ca2+-signalling mechanism by evolutionary developments and transgenic manipulations. Ca2+-signalling appears to be mediated via influx of Ca2+ through the DHP receptor in preference to the Na+-Ca2+ exchange protein, and activates the ryanodine receptor and the Ca2+ release from the SR. Here we report on functional consequences of overexpression of the Na+-Ca2+ exchanger and calsequestrin. The data does not support a physiological role for the Na+-Ca2+ exchanger in signalling Ca2+ release, but can serve to modify ionic currents which determine the duration of the action potential.
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© 1997 Springer Science+Business Media New York
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Morad, M., Suzuki, Y.J. (1997). CA2+-Signaling in Cardiac Myocytes: Evidence from Evolutionary and Transgenic Models. In: Sideman, S., Beyar, R. (eds) Analytical and Quantitative Cardiology. Advances in Experimental Medicine and Biology, vol 430. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5959-7_1
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DOI: https://doi.org/10.1007/978-1-4615-5959-7_1
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