Sage S O, Rink T J
Eur J Pharmacol. 1986 Aug 22;128(1-2):99-107. doi: 10.1016/0014-2999(86)90563-7.
We have investigated the effects of substituting extracellular Na+ by choline or K+ on responses of quin2- and fura-2-loaded human platelets to thrombin and platelet-activating factor (PAF). Na+ substitution by choline did not affect the extent of the rise in [Ca2+]i evoked by either agonist. The response to thrombin, but not PAF, was slightly slowed. High K+ did not activate the cells, but the rises in [Ca2+]i evoked by both agonists were slowed and reduced. Shape change evoked by both agonists was little affected by either substitution. Aggregation evoked by PAF was reduced in high K+ but unaffected in choline. Thrombin-induced aggregation was unaffected by either substitution, even when the rise in [Ca2+]i was markedly reduced. The results suggest that the mechanism which generates Ca2+ fluxes in platelets is not voltage-dependent; but high K+ appears to interfere with the influx mechanism.
我们研究了用胆碱或钾替代细胞外钠离子对负载喹啉-2和fura-2的人血小板对凝血酶和血小板活化因子（PAF）反应的影响。用胆碱替代钠离子不影响两种激动剂引起的细胞内钙离子浓度（[Ca2+]i）升高的程度。对凝血酶的反应略有减慢，但对PAF的反应没有影响。高钾不激活细胞，但两种激动剂引起的[Ca2+]i升高均减慢且幅度减小。两种激动剂引起的形态变化几乎不受任何一种替代的影响。PAF诱导的聚集在高钾环境中减少，但在胆碱环境中不受影响。凝血酶诱导的聚集不受任何一种替代的影响，即使[Ca2+]i的升高明显降低。结果表明，血小板中产生钙离子通量的机制不是电压依赖性的；但高钾似乎会干扰钙离子内流机制。
