On the specificity of verapamil as a calcium channel-blocker

The stimulated uptake of 45Ca2+ into incubated cerebrocortical synaptosomes caused by veratrine (75 microM) was blocked by low concentrations of verapamil (0.5-30 microM) 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 (Ca2+) stores. At higher concentrations (30-200 microM) 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 45Ca2+ influx and neurotransmitter release were prevented by verapamil across a wide concentration range (0.5-200 microM). The data are discussed in terms of the specificity of action of verapamil on Ca2+ channels.