Wiater L A, Dunham P B
Am J Physiol. 1983 Nov;245(5 Pt 1):C348-56. doi: 10.1152/ajpcell.1983.245.5.C348.
Passive transport pathways for K+ and Na+ were studied in fresh human red blood cells (pretreated with ouabain) by measuring unidirectional influxes. The effects of the sulfhydryl binding agents N-ethylmaleimide (NEM) and p-chloromercuribenzene sulfonate (p-CMBS) and the loop diuretic furosemide were studied. Influxes were measured at equimolar K+ and Na+ concentrations (50 mM) with both ions present and also in K+-free or Na+-free media. Some experiments were carried out in Cl--free media (with NO-3 as the substitute). NEM stimulated K+ influx twofold; the stimulation required Cl- but not Na+. NEM inhibited Na+ influx 20%. Furosemide inhibited both K+ and Na+ influxes. All of furosemide-inhibitable Na+ influx required the presence of K+. However 30% of furosemide-inhibitable K+ influx did not require Na+. All of furosemide-inhibitable K+ influx required Cl-. The ratio of Na+-dependent K+ influx to K+-dependent Na+ influx was 3:1. p-CMBS stimulated both Na+ and K+ influxes. K+ influx in p-CMBS cells required neither Na+ nor Cl-. Likewise p-CMBS-promoted Na+ influx did not require K+. These various results are consistent with two Cl--dependent pathways for K+ transport, one requiring Na+ [perhaps (Na + K + Cl) cotransport] and one independent of Na+ [perhaps (K + Cl) cotransport]. The pathways promoted by p-CMBS are probably independent of the apparent cotransport systems.
通过测量单向流入量，研究了新鲜人红细胞（用哇巴因预处理）中钾离子（K⁺）和钠离子（Na⁺）的被动转运途径。研究了巯基结合剂N - 乙基马来酰亚胺（NEM）和对氯汞苯磺酸盐（p - CMBS）以及袢利尿剂速尿的作用。在等摩尔浓度的K⁺和Na⁺（50 mM）同时存在的情况下，以及在无K⁺或无Na⁺的培养基中测量流入量。一些实验在无氯离子（Cl⁻）的培养基（用硝酸根离子（NO₃⁻）替代）中进行。NEM使K⁺流入量增加两倍；这种刺激需要Cl⁻但不需要Na⁺。NEM抑制Na⁺流入量20%。速尿抑制K⁺和Na⁺的流入量。所有速尿可抑制的Na⁺流入都需要K⁺存在。然而，30%的速尿可抑制的K⁺流入不需要Na⁺。所有速尿可抑制的K⁺流入都需要Cl⁻。依赖Na⁺的K⁺流入与依赖K⁺的Na⁺流入的比例为3:1。p - CMBS刺激Na⁺和K⁺的流入量。p - CMBS处理的细胞中的K⁺流入既不需要Na⁺也不需要Cl⁻。同样，p - CMBS促进的Na⁺流入不需要K⁺。这些不同的结果与两种依赖Cl⁻的K⁺转运途径一致，一种需要Na⁺[可能是（Na⁺ + K⁺ + Cl⁻）共转运]，一种不依赖Na⁺[可能是（K⁺ + Cl⁻）共转运]。p - CMBS促进的途径可能独立于明显的共转运系统。
