人红细胞中氯离子激活的被动钾转运
Chloride-activated passive potassium transport in human erythrocytes.
作者信息
Dunham P B, Stewart G W, Ellory J C
出版信息
Proc Natl Acad Sci U S A. 1980 Mar;77(3):1711-5. doi: 10.1073/pnas.77.3.1711.
Abstract
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 . liter-1, hr-1; 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 . liter-1 . hr-1). 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.
摘要
在人类红细胞中，被动钾离子转运（定义为哇巴因不敏感转运）在氯离子被几种渗透性单价阴离子取代时受到70%的抑制。依赖氯离子的钾离子内流的Vmax为1.14 mmol·升⁻¹·小时⁻¹；其对钾离子的表观Km为4.7 mM。存在一个依赖氯离子的钠离子内流的小得多的组分（Vmax，0.23 mmol·升⁻¹·小时⁻¹）。呋塞米和其他氯离子转运抑制剂对被动钾离子转运的抑制程度与氯离子被取代时相同，但4-乙酰氨基-4'-异硫氰基芪-2,2'-二磺酸，一种红细胞阴离子交换的特异性抑制剂，无效。依赖氯离子的钾离子转运，可能是钾离子/氯离子共转运，可能反映了一种调节细胞体积的机制。
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