MacIntyre D E, Shaw A M
Thromb Res. 1983 Sep 15;31(6):833-44. doi: 10.1016/0049-3848(83)90114-7.
Human platelet activation (aggregation, [14C]-5HT release and TxB2 production) induced by the phospholipids, PAF and lysophosphatidic acid (LPA) was inhibited by EGTA, TMB-8 (an intracellular calcium antagonist) and by phenylalkylamine (Class II) but not 1,4-dihydropyridine (Class I) calcium channel blockers. Primary aggregation induced by PAF was selectively inhibited by phenylalkylamine (verapamil, methoxyverapamil) calcium channel blockers. Phospholipid-induced human platelet activation depends predominantly on the influx of extracellular calcium, possibly via specific receptor-operated calcium channels.
由磷脂、血小板活化因子(PAF)和溶血磷脂酸(LPA)诱导的人血小板活化(聚集、[14C]-5-羟色胺释放和血栓素B2生成)受到乙二醇双四乙酸(EGTA)、TMB-8(一种细胞内钙拮抗剂)和苯烷基胺(II类)的抑制,但不受1,4-二氢吡啶(I类)钙通道阻滞剂的抑制。PAF诱导的初级聚集被苯烷基胺(维拉帕米、甲氧维拉帕米)钙通道阻滞剂选择性抑制。磷脂诱导的人血小板活化主要依赖细胞外钙的内流,可能是通过特定的受体操纵性钙通道。