Glusa E, Bevan J, Heptinstall S
Department of Pharmacology, Medical Academy, Erfurt, G.D.R.
Thromb Res. 1989 Jul 15;55(2):239-245. doi: 10.1016/0049-3848(89)90441-6.
We have studied the effects of verapamil, diltiazem and amlodipine on 5-HT-induced platelet aggregation and compared the results with those obtained for other platelet aggregating agents. Experiments were carried out using both human whole blood and platelet-rich plasma (PRP). Verapamil (but not diltiazem or amlodipine) inhibited 5-HT-induced platelet aggregation at much lower concentrations (IC50 = about 1 microM) than were required for inhibition of aggregation induced by other aggregating agents. Like some other selective inhibitors of 5-HT-induced platelet aggregation, it was not possible to completely overcome the inhibition by increasing the concentration of 5-HT. The antiaggregatory effects of verapamil were similar, but not identical, in whole blood and PRP. These results show that the Ca2+ channel blocker verapamil has some selectivity as an inhibitor of 5-HT-induced platelet aggregation and that this behaviour as a 5-HT antagonist should be taken into account when interpreting any therapeutic benefit ascribed to this drug.
我们研究了维拉帕米、地尔硫䓬和氨氯地平对5-羟色胺(5-HT)诱导的血小板聚集的影响,并将结果与其他血小板聚集剂的结果进行了比较。实验使用人体全血和富血小板血浆(PRP)进行。维拉帕米(而非地尔硫䓬或氨氯地平)在比抑制其他聚集剂诱导的聚集所需浓度低得多的浓度(IC50 = 约1微摩尔)下就能抑制5-HT诱导的血小板聚集。与其他一些5-HT诱导的血小板聚集的选择性抑制剂一样,通过增加5-HT的浓度无法完全克服这种抑制作用。维拉帕米在全血和PRP中的抗聚集作用相似但不完全相同。这些结果表明,钙通道阻滞剂维拉帕米作为5-HT诱导的血小板聚集抑制剂具有一定的选择性,在解释归因于该药物的任何治疗益处时,应考虑其作为5-HT拮抗剂的这种行为。