Calcium blocker diltiazem inhibits platelet activation and stimulates vascular prostacyclin synthesis.
The effects of slow channel calcium blocker diltiazem on platelet aggregation and on the generation of vasoactive prostanoids, thromboxane A2 and prostacyclin were examined. Diltiazem, in therapeutic concentrations (50-200 ng/ml), inhibited human platelet activation induced by cumulative subthreshold concentrations of calcium ionophore A 23187 plus ADP or epinephrine. However, platelet activation induced by cumulative effects of ADP plus epinephrine was inhibited by diltiazem only in very high concentrations (greater than 5 micrograms/ml). These data indicate that platelet aggregation mediated only through calcium flux is inhibited by diltiazem in therapeutic concentrations. In other experiments, diltiazem significantly potentiated prostacyclin release from human umbilical veins. These effects of diltiazem may contribute to efficacy of this compound in ischemic heart disease.
D001552:Benzazepines / Q000494:pharmacology*; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism; D004110:Diltiazem / Q000494:pharmacology*; D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects*; D013928:Thromboxane A2 / Q000096:biosynthesis*; D014471:Umbilical Veins / Q000187:drug effects / Q000378:metabolism
D001552:Benzazepines; D013928:Thromboxane A2; D011464:Epoprostenol; D004110:Diltiazem