Dunn M J
J Clin Invest. 1970 Oct;49(10):1804-14. doi: 10.1172/JCI106398.
Active sodium transport (outflux or efflux) in red blood cells generally has been measured by assessing the amount of outflux inhibited by digitalis glycosides (outflux-fraction I). The presence of a ouabain-uninhibited sodium outflux (outflux-fraction II) attributable either to a second active transport mechanism or to exchange diffusion has been the subject of recent investigations. In the present study a variety of transport inhibitors, including ouabain, ethacrynic acid, furosemide, oligomycin, and amiloride, were studied for their effects on these components of sodium transport in RBC. In the presence of ouabain both ethacrynic acid and furosemide exerted similar effects on sodium outflux, inhibiting approximately 0.5 mmoles/L of cells per hr. This component of sodium outflux has been called outflux-fraction II. Ethacrynic acid showed no inhibitory potency when ouabain and furosemide were present, thereby suggesting that the same outflux component (fraction II) was affected by ethacrynic acid and by furosemide. In addition, furosemide reduced sodium influx to the same extent that it reduced sodium outflux. Outflux-fraction II, as defined by furosemide, did not contribute a net sodium outflux. These results of sodium outflux and influx experiments confirm the existence of a transport pathway which does not contribute to net flux and which fits the definition of exchange diffusion. The inhibitory effect of furosemide on outflux-fraction II remained despite the use of a sulfhydryl protective reagent, whereas the effect of ethacrynic acid was obliterated. No combination of inhibitors was found which affected the residual or uninhibited sodium outflux (0.4-0.5 mmoles/liter of cells per hr). Oligomycin possessed an inhibitory potency less than that of ouabain, and it exerted no effect on sodium outflux if it was superimposed upon ouabain inhibition. Amiloride proved to be a very weak inhibitor of sodium outflux in human erythrocytes.
红细胞中的主动钠转运（外流或流出）通常通过评估洋地黄糖苷抑制的外流量（外流部分I）来测量。由第二种主动转运机制或交换扩散引起的哇巴因不敏感钠外流（外流部分II）的存在是最近研究的主题。在本研究中，研究了包括哇巴因、依他尼酸、呋塞米、寡霉素和氨氯吡咪在内的多种转运抑制剂对红细胞中钠转运这些成分的影响。在存在哇巴因的情况下，依他尼酸和呋塞米对钠外流具有相似的作用，每小时抑制约0.5 mmol/L的细胞。这种钠外流成分被称为外流部分II。当存在哇巴因和呋塞米时，依他尼酸没有抑制作用，因此表明依他尼酸和呋塞米影响相同的外流成分（部分II）。此外，呋塞米降低钠内流的程度与降低钠外流的程度相同。由呋塞米定义的外流部分II没有产生净钠外流。这些钠外流和内流实验的结果证实了存在一种对净通量没有贡献且符合交换扩散定义的转运途径。尽管使用了巯基保护剂，呋塞米对外流部分II的抑制作用仍然存在，而依他尼酸的作用则被消除。没有发现影响残余或未抑制钠外流（每小时0.4 - 0.5 mmol/L细胞）的抑制剂组合。寡霉素的抑制效力小于哇巴因，如果在哇巴因抑制的基础上叠加使用，它对钠外流没有影响。氨氯吡咪被证明是人类红细胞中钠外流的一种非常弱的抑制剂。
