PMID: 6411841Sep 1, 1983Paper

Inhibitory effects of diltiazem on platelet activation caused by ionophore A23187 plus ADP or epinephrine in subthreshold concentrations

The Journal of Laboratory and Clinical Medicine
P MehtaL Brigmon

Abstract

We examined the effects of the slow channel Ca++ blocker diltiazem on human platelet aggregation and TXA2 generation. Diltiazem inhibited platelet aggregation induced by 2 microM ADP or 5.5 microM epinephrine alone at 5 and 50 micrograms/ml (11.1 and 111 microM), respectively, and that induced by threshold concentrations of ADP or epinephrine at 0.2 to 1.0 micrograms/ml (0.4 to 2.2 microM). Platelet TXA2 generation stimulated by either ADP or epinephrine alone was inhibited by diltiazem in concentrations above the clinically achieved range (0.05 to 0.2 micrograms/ml, 0.1 to 0.4 microM). When PRP was stimulated with subthreshold concentrations of the Ca++ ionophore A23187 followed by subthreshold concentrations of ADP or epinephrine, a marked potentiation of platelet aggregation and TXA2 generation was observed. Incubation of PRP with diltiazem in a pharmacologic range resulted in marked reduction in ionophore A23187-induced potentiation of platelet activity caused by ADP or epinephrine. In other experiments, diltiazem was found to have no effects on PGI2-induced platelet aggregation inhibition. On the basis of these data, we conclude that (1) Ca++ flux across the platelet membrane stimulates platelet activity of subthreshold co...Continue Reading

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