Gunn R B, Dalmark M, Tosteson D C, Wieth J O
J Gen Physiol. 1973 Feb;61(2):185-206. doi: 10.1085/jgp.61.2.185.
The efflux of chloride-36 from human erythrocytes under steady-state conditions is a saturable process that is competitively inhibited by bicarbonate and noncompetitively inhibited by acetate. This chloride self-exchange flux is reversibly dependent on the pH of the medium between 5.7 and 9.6 with a maximum flux at pH 7.8. The increase in chloride flux between pH 5.7 and 7.8 is inexplicable by the fixed charge hypothesis. The interpretations are made that chloride transport in human erythrocytes is carrier mediated, that bicarbonate utilizes the same transport mechanism, and that the mechanism can be titrated with hydrogen ions into less functional forms for chloride transport.
在稳态条件下,氯-36从人红细胞中的流出是一个可饱和的过程,该过程受到碳酸氢盐的竞争性抑制和乙酸盐的非竞争性抑制。这种氯的自我交换通量在5.7至9.6的介质pH范围内可逆地依赖于介质的pH值,在pH 7.8时通量最大。在pH 5.7至7.8之间氯通量的增加无法用固定电荷假说来解释。由此得出的解释是,人红细胞中的氯转运是由载体介导的,碳酸氢盐利用相同的转运机制,并且该机制可以用氢离子滴定成功能较弱的氯转运形式。