Abstract
In rabbit platelets, the Ca 2+-antagonists, Verapamil and Diltiazem, and the calmodulin inhibitor, Trifluoperazine, inhibited platelet aggregation induced by the mediators of the three pathways platelet-activating factor (Paf-acether), arachidonic acid (AA) and adenosine diphosphate (ADP). The Paf-acether pathway was the most markedly influenced by Verapamil (IC50 = 23 ± 12 μM) and it was the only one to be inhibited by Diltiazem (IC50 = 13 ± 6μM). Trifluoperazine inhibited predominantly the ADP pathway (IC50 = 1 ± 5 μM). Inhibitions were not reversed by increasing Ca 2+ concentrations from 1.4 to 14.2 mM but in the case of Paf-acether were suppressed after removal of Verapamil and Diltiazem but not of Trifluoperazine. Platelets aggregated by Paf-acether, AA and ADP were immediately desaggregated upon addition of each drug. The potency of their anti-aggregating activity was close to that of their vasodilator activity suggesting that Ca 2+-antagonism is the cause of the platelet aggregation inhibition.
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