Verapamil inhibits platelet aggregation by a calcium-independent mechanism.
We studied the inhibitory effects of the calcium channel blocker verapamil both on platelet aggregation and intracellular calcium [Ca2+]i in platelets loaded with a fluorescent indicator (quin 2). The inhibitory effects of verapamil on the platelet aggregation response to both thrombin and ionomycin were seen to be clearly dissociated from the verapamil-induced inhibition of the [Ca2+]i increase produced by these agonists. Verapamil-induced inhibition of platelet aggregation was also obtained when using the "calcium-independent" agonist phorbol-myristate acetate (PMA). It may be deduced that a calcium-independent mechanism plays a role in verapamil-induced inhibition of platelet aggregation. We postulate that this mechanism may operate via a protein-kinase C pathway.
D002118:Calcium / Q000502:physiology*; D004987:Ethers / Q000494:pharmacology; D006801:Humans; D007473:Ion Channels / Q000187:drug effects; D015759:Ionomycin; D010974:Platelet Aggregation / Q000187:drug effects*; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D013917:Thrombin / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology*
D004987:Ethers; D007473:Ion Channels; D015759:Ionomycin; D014700:Verapamil; D013917:Thrombin; D013755:Tetradecanoylphorbol Acetate; D002118:Calcium