Passive transport of K+ and Na+ in human red blood cells: sulfhydryl binding agents and furosemide.
Passive transport of K+ and Na+ in human red blood cells: sulfhydryl binding agents and furosemide.
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人红细胞中 K 和 Na 的被动转运：巯基结合剂和呋塞米。
DOI：
10.1152/ajpcell.1983.245.5.c348
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Dunham,PB
中科院分区：
文献类型：
--
作者：
Wiater,LA;Dunham,PB
通过测量单向流入，研究了新鲜人红细胞（用哇巴因预处理）中 K+ 和 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) 以及袢利尿剂呋塞米的作用。在两种离子均存在的情况下以及在不含 K+ 或不含 Na+ 的介质中，以等摩尔 K+ 和 Na+ 浓度 (50 mM) 测量流入量。一些实验是在无Cl-培养基（用NO-3作为替代品）中进行的。 NEM 双重刺激 K+ 流入；刺激需要 Cl-，但不需要 Na+。 NEM 抑制 Na+ 内流 20%。呋塞米抑制 K+ 和 Na+ 流入。所有速尿抑制的 Na+ 流入都需要 K+ 的存在。然而，30% 的速尿抑制 K+ 流入不需要 Na+。所有呋塞米抑制的 K+ 内流都需要 Cl-。 Na+依赖的K+内流与K+依赖的Na+内流之比为3:1。 p-CMBS 刺激 Na+ 和 K+ 流入。 p-CMBS 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 K+ 转运的两种 Cl-依赖性途径一致，一种需要 Na+ [可能 (Na + K + Cl) 共转运]，另一种独立于 Na+ [可能 (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。
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.