Abstract
In cardiac and skeletal muscle excitation-contraction coupling is dependent upon release of calcium (Ca2+) from junctional sarcoplasmic reticulum via a ryanodine-sensitive Ca2+-release channel. Similar oscillatory changes in intracellular Ca2+ concentration are important for the normal function of neutrophils. Therefore, we postulated the existence of a ryanodine-sensitive Ca2+ channel in human neutrophils. This hypothesis is supported by our prior observation that ryanodine (10 nM) increased the intracellular Ca2+ content of intact human neutrophils1.
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References
D.P. Rardon, and L.P. Akard, Ryanodine regulation of intracellular calcium and divalent cation channel activity in human neutrophils, Circulation, 80:II–519, (1989).
T.G. Gabig, D. English, L.P. Akard, and M.J. Schell, Regulation of neutrophil NADPH oxidase activation in a cell-free system by guanine nucleotides and fluoride, J. Biol. Chem., 262:1685–1690, (1987).
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© 1992 Springer Science+Business Media New York
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Rardon, D.P., Krause, P.C. (1992). Purification of a Ryanodine-Sensitive Channel Protein from Human Neutrophils. In: Frank, G.B., Bianchi, C.P., ter Keurs, H.E.D.J. (eds) Excitation-Contraction Coupling in Skeletal, Cardiac, and Smooth Muscle. Advances in Experimental Medicine and Biology, vol 311. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3362-7_56
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DOI: https://doi.org/10.1007/978-1-4615-3362-7_56
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