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.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005260:Female; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D014700:Verapamil / Q000494:pharmacology*; D014702:Veratrine / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D005680:gamma-Aminobutyric Acid; D014700:Verapamil; D014702:Veratrine; D011188:Potassium; D002118:Calcium