Kitagawa S, Usui K, Kametani F
Faculty of Pharmaceutical Sciences, University of Tokushima, Japan.
Biochim Biophys Acta. 1989 May 10;1011(2-3):117-21. doi: 10.1016/0167-4889(89)90197-3.
The effects of ionophores, which can carry alkali metal cations, on platelet aggregation were examined. At an alkaline extracellular pH, alkali metal cation/H+ exchanger nigericin accelerated aggregation in K+-enriched medium, whereas it rather inhibited aggregation in Na+-enriched medium, even though the intracellular pH was only slightly alkaline. The inhibitory effect of Na+ on platelet aggregation was more clearly shown with the alkali metal cation exchanger gramicidin D. The ionophore had no effect or a slightly accelerative effect on aggregation in K+-enriched medium, whereas it significantly inhibited aggregation induced by thrombin, ADP and platelet activating factor in Na+-enriched medium. Fluorescence studies on fura-2-labeled platelets revealed that in Na+-enriched medium gramicidin D inhibited agonist-induced Ca2+ mobilization both in the presence and absence of extracellular Ca2+. These results suggest that the intracellular Na+ inhibits platelet aggregation by inhibiting Ca2+ mobilization.
研究了可携带碱金属阳离子的离子载体对血小板聚集的影响。在碱性细胞外pH值下,碱金属阳离子/H⁺交换剂尼日利亚菌素在富含K⁺的培养基中加速聚集,而在富含Na⁺的培养基中则抑制聚集,尽管细胞内pH值仅略呈碱性。用碱金属阳离子交换剂短杆菌肽D能更清楚地显示Na⁺对血小板聚集的抑制作用。该离子载体在富含K⁺的培养基中对聚集无作用或有轻微的促进作用,而在富含Na⁺的培养基中它能显著抑制凝血酶、ADP和血小板活化因子诱导的聚集。对用fura-2标记的血小板的荧光研究表明,在富含Na⁺的培养基中,短杆菌肽D在有或无细胞外Ca²⁺存在的情况下均抑制激动剂诱导的Ca²⁺动员。这些结果表明,细胞内Na⁺通过抑制Ca²⁺动员来抑制血小板聚集。