Abstract
A RECENT hypothesis about the mechanism of action of procaine and structurally similar depressants of excitation emphasizes their interaction with membrane calcium1. Procaine, it is suggested, replaces calcium at membrane anionic sites and this inhibits the influence of excitable stimuli on processes leading to sodium influx. The hypothesis is based, in part, on the assumed role of calcium in excitation, for the release of this cation is widely viewed as the first important step in membrane depolarization2. Furthermore, high concentrations of external calcium oppose the action of procaine on frog motoneurones3 and lobster giant axons1. Evidence that procaine or other local anaesthetics actually increase the mobility of membrane calcium has not yet been reported. I have investigated the interaction between procaine and calcium in nerve and muscle and the question of whether procaine causes the calcium to be released from these tissues.
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References
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KUPERMAN, A., ALTURA, B. & CHEZAR, J. Action of Procaine on Calcium Efflux from Frog Nerve and Muscle. Nature 217, 673–675 (1968). https://doi.org/10.1038/217673a0
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DOI: https://doi.org/10.1038/217673a0
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