Bakker-Grunwald T, Keller F, Trissl D
Biochim Biophys Acta. 1986 Jan 29;854(2):265-9. doi: 10.1016/0005-2736(86)90119-7.
Amiloride, a blocker of Na+ leak and Na+-H+ exchange in animal cells, caused cells of Entamoeba histolytica to release Na+ (up to 40% of their original Na+ content within 90 min, at an amiloride concentration of 3 mM); K+ content was not affected. By comparing the unidirectional uptake of 22Na+ with that of the fluid-phase marker 125I-labeled poly(vinylpyrrolidone) we established that the amiloride-induced Na+ loss was due to inhibition of pinocytic Na+ uptake rather than to blockage of an amiloride-sensitive transport system in the plasma membrane. Amiloride penetrated the cells, and both its intracellular concentration and its effect on pinocytosis increased with pH. The permeant weak base quinacrine similarly inhibited pinocytosis in a pH-dependent manner. We conclude that the effect of amiloride on pinocytosis and, consequently, on Na+ content was due to its properties as a permeant weak base.
氨氯吡咪是动物细胞中Na⁺渗漏和Na⁺-H⁺交换的阻滞剂，它能使溶组织内阿米巴细胞释放Na⁺（在氨氯吡咪浓度为3 mM时，90分钟内可释放其原有Na⁺含量的40%）；K⁺含量不受影响。通过比较²²Na⁺的单向摄取与液相标记物¹²⁵I标记的聚（乙烯基吡咯烷酮）的摄取，我们确定氨氯吡咪诱导的Na⁺损失是由于抑制了胞饮性Na⁺摄取，而不是由于阻断了质膜中对氨氯吡咪敏感的转运系统。氨氯吡咪可穿透细胞，其细胞内浓度及其对胞饮作用的影响均随pH值升高而增加。渗透性弱碱喹吖因同样以pH依赖的方式抑制胞饮作用。我们得出结论，氨氯吡咪对胞饮作用以及对Na⁺含量的影响是由于其作为渗透性弱碱的特性。
