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- W1967098981 abstract "The effects of pyrethroids were studied on K+-stimulated 45Ca2+ uptake by rat brain synaptosomes. This uptake had low affinity for the inhibitors of voltage-dependent Ca2+ channels (verapamil, diltiazem, nimodipine, and nifedipine) but was potently inhibited by 2′-4′-dichlorobenzamil (DCB). The characteristics of 45Ca2+ uptake, measured in the absence of any added ATP, suggested that most of it was a result of the activity of the Na+-Ca2+ exchanger in these membranes. The pyrethroids were more potent inhibitors of this K+-stimulated 45Ca2+ uptake than even the “specific” inhibitor DCB. The seven type II pyrethroids (containing α-cyano-3-phenoxybenzyl alcohol) tested (with average IC50 of 11 μM) were more potent inhibitors of this 45Ca2+ uptake than the seven type I pyrethroids (which do not contain an α-cyano substituent). Both toxic and nontoxic cypermethrin isomers inhibited the 45Ca2+ uptake with similar potencies. Both types of pyrethroids also inhibited voltage-dependent Ca2+ channels in the membrane, which were detected by their specific binding of [3H]nimodipine with the following order of decreasing potencies: pyrethrins>cypermethrin>cyfluthrin>deltamethrin = resmethrin>tetramethrin>S-bioallethrin> allethrin = permethrin>flucythrinate>bioallethrin>fenvalerate = fluvalinate ⪢ tralomethrin. The relatively low potencies of pyrethroids on the K+-stimulated 45Ca2+ uptake and [3H]nimodipine binding, the poor stereospecificity of pyrethroid action, and the poor correlation with their toxicities suggest that neither the Na+-Ca2+ exchanger nor the voltage-dependent Ca2+ channel are primary targets for pyrethroid toxicity." @default.
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- W1967098981 date "1988-10-01" @default.
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- W1967098981 title "Action of pyrethroids on K+-stimulated calcium uptake by, and [3H]nimodipine binding to, rat brain synaptosomes" @default.
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- W1967098981 doi "https://doi.org/10.1016/0048-3575(88)90004-1" @default.
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