Abstract
Ca2+ binding to troponin-C, a regulatory protein of muscle contraction, is an important step for the initiation of cardiac muscle contraction [1]. Therefore, the change in the intracellular Ca2+ concentration ([Ca2+]i) and the affinity of troponin-C for Ca2+ are intimately related to cardiac muscle contraction. In mammalian cardiac muscles, intracellular Ca2+, which initiates contraction, is mainly delivered by the sarcoplasmic reticulum (SR) [2]. Therefore, the factors that influence Ca2+ release from SR are considered to cause the alteration in contraction. In addition, the factors that alter Ca2+ uptake by SR also influence the magnitude and the time course of intracellular Ca2+ transients.
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Kurihara, S., Komukai, K., Kawai, M., Tanaka, E., Konishi, M. (1996). Intracellular Ca2+ Transients in Response to Step Length Changes in Aequorin-Injected Ferret Papillary Muscles. In: Dhalla, N.S., Singal, P.K., Takeda, N., Beamish, R.E. (eds) Pathophysiology of Heart Failure. Developments in Cardiovascular Medicine, vol 168. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1235-2_16
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DOI: https://doi.org/10.1007/978-1-4613-1235-2_16
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