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Nitric Oxide and Voltage-Gated Ca2+ Channels

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Signal Transduction and the Gasotransmitters

Summary

Nitric oxide (NO) markedly influences intracellular calcium homeostasis by affecting the influx of Ca2+ through the plasma membrane and its release from intracellular stores. There is a large body of experimental evidence indicating that all mechanisms controlling the intracellular Ca2+ concentrations are regulated by NO. In excitable cells, activation of the voltage-gated Ca2+ channels is certainly the most effective means of generating Ca2+ influx from the extracellular space in response to membrane depolarization, and Ca2+ passing through these channels is known to regulate fundamental cellular functions, including neurotransmitter release, heart and smooth muscle contraction, synthesis and modulation of intracellular enzymes, regulation of gene expression, cell proliferation, and apoptosis. This chapter reviews numerous studies highlighting direct and indirect modulatory effects of NO on various types of voltage-gated Ca2+ channels and discusses the functional implications of the interaction of NO with voltage-gated Ca2+ channels.

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Grassi, C., D’Ascenzo, M., Azzena, G.B. (2004). Nitric Oxide and Voltage-Gated Ca2+ Channels. In: Wang, R. (eds) Signal Transduction and the Gasotransmitters. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-806-9_7

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