On the specificity of verapamil as a calcium channel-blocker

Abstract

The stimulated uptake of 45Ca 2+ into incubated cerebrocortical synaptosomes caused by veratrine (75 μM) was blocked by low concentrations of verapamil (0.5–30 μM) which did not prevent or reduce depolarization as judged by efflux of potassium (K +). However, verapamil did not prevent amino acid neutrotransmitter release at these low concentrations and this is discussed in terms of mobilization of internal calcium (Ca 2+) stores. At higher concentrations (30–200 μM) verapamil appeared to act additionally at sodium (Na −) channels since both depolarization-induced K + efflux and neurotransmitter release were reduced or prevented. When K +, at a high concentration (56 mM), was used as the depolarizing agent, both 45Ca 2+ influx and neurotransmitter release were prevented by verapamil across a wide concentration range (0.5–200 μM). The data are discussed in terms of the specificity of action of verapamil on Ca 2+ channels.