Activation of sodium–proton exchange is a prerequisite for Ca2+ mobilization in human platelets
Activation of sodium–proton exchange is a prerequisite for Ca2+ mobilization in human platelets
复制标题
钠质子交换的激活是人血小板中 Ca2+ 动员的先决条件
作者：
W. Siffert;J. Akkerman
受刺激的血小板吸收钠离子1，2并释放氢离子3，这是由于Na +/H+交换的激活4，5导致细胞质碱化6。通过去除细胞外Na+或通过应用阿米洛利抑制Na +/H+交换抑制形状变化、颗粒内容物的分泌和聚集5，7 - 9。我们在这里提出的数据表明，抑制这种运输乙基异丙基阿米洛利或通过降低细胞外钠减少，甚至完全抑制细胞质游离Ca2+浓度的上升，这是必不可少的血小板聚集在凝血酶的反应。我们还表明，暴露于离子载体莫能菌素产生的细胞质碱化敏感的人血小板对凝血酶刺激的反应，从而增强Ca2+动员和聚集性。我们的结论是，在细胞内pH值的增加引起的激活Na +/H+计数器运输是一个重要的信号，在刺激-反应耦合，并形成一个必要的步骤，在级联事件所需的增加血小板细胞质游离钙。
Stimulated platelets take up sodium ions1,2 and release hydrogen ions3 due to activation of Na+/H+ exchange4,5 resulting in cytoplasmic alkalinization6. Suppression of Na+/H+ exchange either by removal of extracellular Na+ or by application of amiloride inhibits shape change, secretion of granule contents and aggregation5,7–9. The data we present here indicate that inhibition of this transport by ethylisopropyl-amiloride or by lowering extracellular sodium reduces or even completely suppresses the rise in cytoplasmic free Ca2+ concentration that is essential for platelet aggregation in response to thrombin. We also demonstrate that cytoplasmic alkalinization produced by exposure to the ionophore monensin sensitizes the human platelet response to stimulation by thrombin resulting in enhanced Ca2+ mobilization and aggregability. We conclude that an increase in intracellular pH evoked by activation of Na+/H+ counter transport is an important signal in stimulus–response coupling and forms an essential step in the cascade of events required to increase cytoplasmic free Ca2+ in platelets.