Abstract
Intracellular calcium ions play a critical role in many tissues. In many cases, a rise in intracellular calcium is the trigger for one or more cellular functions such as release of neurotransmitters from nerve terminals, control of fertilization, and contraction of most types of muscle cells including skeletal, smooth, and cardiac (Byerly and Hagiwara, 1981). Calcium ions enter cells by moving down their electrochemical gradient through channels in specific transmembrane proteins. In most cases, these channels are voltage gated and open when the membrane is depolarized. In some nerve and muscle cells, an inward calcium current can actually account for regenerative spikes. The calcium channel is a major site for regulation by drugs and hormones. For example, in heart and invertebrate neurons, neurotransmitters, apparently acting via a cAMP-protein phosphorylation cascade, have been shown to regulate calcium channels in the target cells (Reuter, 1983). A number of substances (the so-called “organic calcium antagonists”) have been shown to modify calcium channel activity in excitable cells (Triggle and Janis, 1984). These blockers (e.g., verapamil, nifedipine, and diltiazem) have been used clinically to treat certain cardiac arrhythmias, angina, and hypertension (see Triggle and Janis, 1984). The dihydropyridines appear to be the most exciting of these organic calcium antagonists because of their high potency and their potential as therapeutic agents.
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© 1986 Springer Science+Business Media New York
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Nelson, M.T. (1986). Calcium Channels. In: Miller, C. (eds) Ion Channel Reconstitution. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-1361-9_20
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DOI: https://doi.org/10.1007/978-1-4757-1361-9_20
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