Increase of cGMP and accumulation of 45Ca2+ evoked by drugs acting on sodium or potassium channels

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Abstract

Cyclic guanosine monophosphate (cGMP) and45Ca2+accumulation were measured in mouse cerebellar slices after treatment with compounds known to affect ion channels in excitable membranes. Scorpion toxin and sea anemone toxin II raise cGMP and45Ca2+contents. Both toxins are known to keep the activated sodium channel open. 4-Aminopyridine and tetraethylammonium, which block potassium conductance, also increase cGMP and promote dose-dependently the45Ca2+accumulation. The effects of these 4 drugs but not the effects of depolarizing K+-concentrations on the accumulation of cGMP and45Ca2+are inhibited by tetrodotoxin. The cyclic GMP content of non-excitable cells, such as isolated hepatocytes from rat and guinea pig, is not affected in a comparable manner. We conclude that in excitable cells, sodium influx triggers an increase of intracellular free calcium and in that way a rise of cGMP. This effect is independent of the ion channel primarily affected. Conversely, the concentration of cGMP might serve as an indicator of intracellular free calcium. © 1981.

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Ahnert-Hilger, G., & Habermann, E. (1981). Increase of cGMP and accumulation of 45Ca2+ evoked by drugs acting on sodium or potassium channels. European Journal of Pharmacology, 70(3), 301–310. https://doi.org/10.1016/0014-2999(81)90164-3

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