CHLORIDE-ACTIVATED PASSIVE POTASSIUM-TRANSPORT IN HUMAN-ERYTHROCYTES
CHLORIDE-ACTIVATED PASSIVE POTASSIUM-TRANSPORT IN HUMAN-ERYTHROCYTES
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DOI：
10.1073/pnas.77.3.1711
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发表时间：
1980-01-01
期刊：
影响因子：
--
通讯作者：
ELLORY, JC
中科院分区：
文献类型：
--
作者：
DUNHAM, PB;STEWART, GW;ELLORY, JC
人红细胞被动K+转运（定义为哇巴因不敏感的运输）被抑制70%的几个渗透性单价阴离子的Cl-取代。Cl-依赖性K+内流的Vmax为1.14mmol·cm-1。L ~（-1）/h，K ~+的表观Km为4.7mM，Na ~+内流中Cl ~-依赖的组分要小得多（Vmax为0.23mmol·cm ~（-1）/h）。l-1/h）。呋塞米和其他Cl-转运抑制剂抑制被动K+转运的程度与置换Cl-相同，但红细胞阴离子交换的特异性抑制剂4-乙酰氨基-4“-异硫氰基芪-2，2”-二磺酸无效。Cl-依赖的K+转运（可能是K+/Cl-共转运）可能反映了细胞体积调节的一种机制。
Passive K+ transport in human erythrocytes (defined as ouabain-insensitive transport) was inhibited 70% by replacement of Cl- by several permeant monovalent anions. The Vmax of Cl--dependent K+ influx was 1.14 mmol .cntdot. l-1 per h; its apparent Km for K+ was 4.7 mM. There was a much smaller component of Na+ influx dependent on Cl- (Vmax, 0.23 mmol .cntdot. l-1 per h). Furosemide and other inhibitors of Cl- transport inhibited passive K+ transport to the same extent as replacement of Cl-, but 4-acetamido-4''-isothiocyanostilbene-2,2''-disulfonic acid, a specific inhibitor of anion exchange in erythrocytes, was ineffective. The Cl--dependent K+ transport, which may be K+/Cl- cotransport, could reflect a mechanism for regulating cell volume.