Elsevier

Biochemical Pharmacology

Volume 50, Issue 8, 12 October 1995, Pages 1187-1197
Biochemical Pharmacology

Research paper
Maitotoxin-elicited calcium influx in cultured cells: Effect of calcium-channel blockers

https://doi.org/10.1016/0006-2952(95)00257-ZGet rights and content

Abstract

Maitotoxin elicited a marked influx of 45Ca2+ into NIH 3T3 fibroblast cells. The influx was blocked by imidazoles (econazole, miconazole, SKF 96365, clotrimazole, calmidazolium) with ic50 values from 0.56 to 3 μM. Phenylalkylamines (verapamil, methoxyverapamil) and nitrendipine were less potent, and diltiazem was very weak. Among other calcium blockers, the diphenylbutylpiperidines fluspirilene and penfluridol, the diphenylpropylpiperidine loperamide, and the local anesthetic proadifen were quite active with ic50 values of 2–4 μM. The pattern of inhibition of maitotoxin-elicited calcium influx did not correspond to the ability of the agents to block elevation of calcium that ensues through calcium-release activated calcium (CRAC) channels after activation of phosphoinositide breakdown by ATP in HL-60 cells. The imidazoles did block CRAC channels, but fluspirilene, penfluridol, loperamide and proadifen were ineffective. Loperamide actually appeared to enhance influx of calcium via the activated CRAC channels. The imidazoles, in particular calmidazolium, caused an apparent influx of calcium and caused a stimulation of phosphoinositide breakdown in HL-60 cells.

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Current address: Eisai Research Institute, Andover, MA.

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