Parker J C
Am J Physiol. 1983 May;244(5):C324-30. doi: 10.1152/ajpcell.1983.244.5.C324.
As dog red blood cells are shrunken in vitro, their sodium permeability increases progressively. Some new features of this volume-responsive transport process are described. Retardation of sodium movements in shrunken cells occurs when chloride is replaced by the more conductive anions: nitrate or thiocyanate. Micromolar concentrations of amiloride or quinidine inhibit the increment of sodium flux associated with a reduction in cell volume. In the presence of a large outwardly directed sodium gradient, dog red blood cells can progressively alkalinize the medium in which they are suspended. This pH change is stimulated by cell shrinkage, reversed by cell swelling, retarded when chloride is replaced by nitrate or thiocyanate, and inhibited by micromolar concentrations of amiloride or quinidine. The similarities between the shrinkage-associated sodium flux and the alkalinization phenomenon suggest that the mechanism responsible for increased sodium permeability in shrunken cells can be made to operate as a sodium-hydrogen exchanger.
当犬红细胞在体外发生皱缩时，其钠通透性会逐渐增加。本文描述了这种体积反应性转运过程的一些新特征。当用传导性更强的阴离子（硝酸盐或硫氰酸盐）取代氯离子时，皱缩细胞中的钠移动会受到阻碍。微摩尔浓度的氨氯吡脒或奎尼丁会抑制与细胞体积减小相关的钠通量增加。在存在较大外向钠梯度的情况下，犬红细胞可使其悬浮的培养基逐渐碱化。这种pH变化受到细胞皱缩的刺激，细胞肿胀可使其逆转，当用硝酸盐或硫氰酸盐取代氯离子时会受到阻碍，并且会被微摩尔浓度的氨氯吡脒或奎尼丁抑制。与皱缩相关的钠通量和碱化现象之间的相似性表明，导致皱缩细胞中钠通透性增加的机制可作为钠-氢交换体发挥作用。
