Effects of verapamil on platelet aggregation, ATP release and thromboxane generation.
We examined the effects of verapamil on platelet function. Verapamil (0.5 micrograms/ml) in this study inhibited platelet aggregation induced by threshold amounts of ADP, AA, and epinephrine. With higher concentrations of aggregating stimuli, verapamil caused a dose-dependent inhibition of aggregation. Verapamil reduced the extent of epinephrine-induced primary wave, but not that by ADP. Ristocetin-induced aggregation was not affected at any concentration of verapamil. Platelet ATP release induced by AA and ADP was also inhibited. In vitro platelet TXA2 generation was inhibited by verapamil in concentrations lower than those required for inhibition of aggregation.
D000255:Adenosine Triphosphate / Q000097:blood*; D000328:Adult; D001792:Blood Platelets / Q000187:drug effects; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects*; D013928:Thromboxane A2 / Q000097:blood*; D013931:Thromboxanes / Q000097:blood*; D014700:Verapamil / Q000494:pharmacology*
D013931:Thromboxanes; D013928:Thromboxane A2; D000255:Adenosine Triphosphate; D014700:Verapamil