Han P, Boatwright C, Ardlie N G
Thromb Haemost. 1983 Aug 30;50(2):513-7.
The effects of the calcium-entry blocking agent nifedipine on the activation of human platelets by various agonists has been studied and compared with verapamil. Like verapamil, nifedipine inhibited platelet aggregation and secretion caused by collagen, the second phase of ADP-induced aggregation, and aggregation caused by the ionophore A23187. Both agents inhibited the formation of TXB2 from endogenous arachidonate, whereas only nifedipine inhibited platelet aggregation and decreased TXB2 formation caused by exogenous arachidonate without inhibiting uptake. These results indicate that both calcium-blocking agents may be inhibiting the release of arachidonate in platelets by phospholipases, and that nifedipine also inhibits the formation and action of thromboxane A2 in platelets. Epinephrine-induced aggregation was inhibited by low concentrations of verapamil while nifedipine only inhibited aggregation by epinephrine at much higher concentrations. It is suggested that low concentrations of verapamil inhibit epinephrine-induced aggregation by interacting with platelet alpha-adrenergic receptors, and that higher concentrations of both calcium-blocking agents inhibit platelet responses to other aggregating agents by preventing intracellular calcium mobilization.
已对钙通道阻滞剂硝苯地平对各种激动剂激活人血小板的作用进行了研究，并与维拉帕米作了比较。与维拉帕米一样，硝苯地平抑制由胶原引起的血小板聚集和分泌、ADP诱导聚集的第二阶段以及离子载体A23187引起的聚集。两种药物均抑制内源性花生四烯酸生成TXB2，而仅硝苯地平抑制外源性花生四烯酸引起的血小板聚集并减少TXB2生成，且不抑制摄取。这些结果表明，两种钙阻滞剂可能都通过磷脂酶抑制血小板中花生四烯酸的释放，并且硝苯地平还抑制血小板中血栓素A2的生成和作用。低浓度的维拉帕米抑制肾上腺素诱导的聚集，而硝苯地平仅在高得多的浓度下才抑制肾上腺素诱导的聚集。提示低浓度的维拉帕米通过与血小板α-肾上腺素能受体相互作用抑制肾上腺素诱导的聚集，而两种钙阻滞剂的高浓度则通过阻止细胞内钙动员来抑制血小板对其他聚集剂的反应。
