Jones G S, Knauf P A
J Gen Physiol. 1985 Nov;86(5):721-38. doi: 10.1085/jgp.86.5.721.
When human erythrocytes are suspended in low-Cl- media (with sucrose replacing Cl-), there is a large increase in both the net efflux and permeability of K+. A substantial portion (greater than 70% with Cl- less than 12.5 mM) of this K+ efflux is inhibited by the anion exchange inhibitor DIDS (4,4'-diisothiocyanostilbene-2,2'-disulfonic acid). This inhibition cannot be explained as an effect of DIDS on net Cl- permeability (Pcl) and membrane potential, but rather represents a direct effect on the K+ permeability. When cells are reacted with DIDS for different times, the inhibition of K+ efflux parallels that of Cl- exchange, which strongly indicates that the band 3 anion exchange protein (capnophorin) mediates the net K+ flux. Since a noncompetitive inhibitor of anion exchange, niflumic acid, has no effect on net K+ efflux, the net K+ flow does not seem to involve the band 3 conformational change that mediates anion exchange. The data suggest that in low-Cl- media, the anion selectivity of capnophorin decreases so that it can act as a very low-conductivity channel for cations. Na+ and Rb+, as well as K+, can utilize this pathway.
当人类红细胞悬浮于低氯介质（用蔗糖替代氯离子）中时，钾离子的净外流和通透性均大幅增加。这种钾离子外流的很大一部分（当氯离子浓度低于12.5 mM时，超过70%）会被阴离子交换抑制剂DIDS（4,4'-二异硫氰基芪-2,2'-二磺酸）抑制。这种抑制作用不能解释为DIDS对氯离子净通透性（Pcl）和膜电位的影响，而更像是对钾离子通透性的直接作用。当细胞与DIDS反应不同时间时，钾离子外流的抑制与氯离子交换的抑制情况相似，这有力地表明带3阴离子交换蛋白（碳酸酐酶）介导了钾离子的净通量。由于阴离子交换的非竞争性抑制剂氟尼辛对钾离子净外流没有影响，钾离子的净流动似乎不涉及介导阴离子交换的带3构象变化。数据表明，在低氯介质中，碳酸酐酶的阴离子选择性降低，从而使其能够作为一种极低电导率的阳离子通道发挥作用。钠离子、铷离子以及钾离子都可以利用这条途径。
