Palés J, Palacios-Araus L, López A, Gual A
Laboratori de Neurofisiologia i Biomembranes, Facultat de Medicina, Universitat de Barcelona, Spain.
Biochim Biophys Acta. 1989 Mar 27;980(1):33-6. doi: 10.1016/0005-2736(89)90196-x.
The effects of extracellular Na+ and tetrodotoxin on resting membrane potential, cytosolic free Ca2+ levels and aggregation of human platelets have been studied. Neither the decrease in extracellular Na+-concentration (from 140 mmol/l to 0 mmol/l) nor the addition of tetrodotoxin (10(-7) to 10(-5) mol/l) modified the platelet membrane potential. Zero extracellular Na+ concentration or the presence of tetrodotoxin in the medium inhibited platelet aggregation; however, K+-depolarized platelets showed an unchanged aggregation induced by ADP or thrombin in media with zero or low extracellular Na+ concentrations or in the presence of tetrodotoxin. Moreover, zero extracellular Na+ concentration or tetrodotoxin inhibited calcium mobilization in platelets during activation induced by thrombin. Hence, voltage-dependent activation linked to Na+ influx appears to be necessary for ADP- and thrombin-induced platelet aggregation under control conditions. Mechanisms for the role of Na+ conductances in platelet function are discussed.
研究了细胞外钠离子（Na⁺）和河豚毒素对人血小板静息膜电位、胞质游离钙离子（Ca²⁺）水平及聚集的影响。细胞外Na⁺浓度降低（从140 mmol/L降至0 mmol/L）或添加河豚毒素（10⁻⁷至10⁻⁵ mol/L）均未改变血小板膜电位。细胞外Na⁺浓度为零或培养基中存在河豚毒素会抑制血小板聚集；然而，在细胞外Na⁺浓度为零或较低浓度的培养基中或存在河豚毒素的情况下，K⁺去极化的血小板对ADP或凝血酶诱导的聚集反应不变。此外，细胞外Na⁺浓度为零或河豚毒素会抑制凝血酶诱导激活过程中血小板的钙动员。因此，在对照条件下，与Na⁺内流相关的电压依赖性激活似乎是ADP和凝血酶诱导血小板聚集所必需的。文中讨论了Na⁺电导在血小板功能中作用的机制。
