泽蛙红细胞中的钾离子转运：钾-氯协同转运的证明

Potassium transport in red blood cells of frog Rana temporaria: demonstration of a K-Cl cotransport.

作者信息

Gusev G P, Agalakova N I, Lapin A V

机构信息

Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg.

出版信息

J Comp Physiol B. 1995;165(3):230-7. doi: 10.1007/BF00260814.

DOI:10.1007/BF00260814

PMID:7665736

Abstract

Pathways of K+ movement across the erythrocyte membrane of frog Rana temporaria were studied using 86Rb as a tracer. The K+ influx was significantly blocked by 0.1 mmol.l-1 ouabain (by 30%) and 1 mmol.l-1 furosemide (by 56%) in the red cells incubated in saline at physiological K+ concentration (2.7 mmol.l-1). Ouabain and furosemide had an additive effect on K+ transport in frog red cells. The ouabain-sensitive and furosemide-sensitive components of K+ influx saturated as f(K+)e with apparent Km values for external Ke+ concentration of 0.96 +/- 0.11 and 4.6 +/- 0.5 mmol.l-1 and Vmax of 0.89 +/- 0.04 and 2.8 +/- 0.4 mmol.l cells-1.h-1, respectively. The residual ouabain-furosemide-resistant component was also a saturable function of Ke+ medium concentration. Total K+ influx was significantly reduced when frog erythrocytes were incubated in NO3- medium. Furosemide did not affect K+ transport in frog red cells in NO3- media. At the same Ke+ concentration the ouabain-furosemide-insensitive K+ influx in Cl- medium was significantly greater than that in NO3- medium. We found no inhibitory effect of 1 mmol.l-1 furosemide on Na+ influx in frog red cells in Cl- medium. K+ loss from the frog erythrocytes in a K(+)-free medium was significantly reduced (mean 58%) after replacement of Cl- with NO3-. Furosemide (0.5 mmol.l-1) did not produce any significant reduction in the K+ loss in both media. The Cl(-)-dependent component of K+ loss from frog red cells was 5.7 +/- 1.2 mmol.l-1.h-1.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

以⁸⁶Rb作为示踪剂，研究了K⁺跨蛙（泽蛙）红细胞膜的转运途径。在生理K⁺浓度（2.7 mmol·L⁻¹）的盐溶液中孵育的红细胞中，0.1 mmol·L⁻¹哇巴因（抑制30%）和1 mmol·L⁻¹呋塞米（抑制56%）可显著阻断K⁺内流。哇巴因和呋塞米对蛙红细胞的K⁺转运有相加作用。K⁺内流中对哇巴因敏感和对呋塞米敏感的成分随外部K⁺浓度f(K⁺)e饱和，外部K⁺浓度的表观Km值分别为0.96±0.11和4.6±0.5 mmol·L⁻¹，Vmax分别为0.89±0.04和2.8±0.4 mmol·L⁻¹细胞⁻¹·h⁻¹。剩余的对哇巴因 - 呋塞米不敏感的成分也是K⁺介质浓度的饱和函数。当蛙红细胞在NO₃⁻介质中孵育时，总K⁺内流显著降低。呋塞米不影响蛙红细胞在NO₃⁻介质中的K⁺转运。在相同的K⁺浓度下，Cl⁻介质中对哇巴因 - 呋塞米不敏感的K⁺内流显著大于NO₃⁻介质中的。我们发现1 mmol·L⁻¹呋塞米对Cl⁻介质中蛙红细胞的Na⁺内流没有抑制作用。用NO₃⁻替代Cl⁻后，蛙红细胞在无K⁺介质中的K⁺流失显著减少（平均减少58%）。呋塞米（0.5 mmol·L⁻¹）在两种介质中均未使K⁺流失产生任何显著减少。蛙红细胞K⁺流失的Cl⁻依赖性成分是5.7±1.2 mmol·L⁻¹·h⁻¹。（摘要截短于250字）