Ellory J C, Dunham P B, Logue P J, Stewart G W
Philos Trans R Soc Lond B Biol Sci. 1982 Dec 1;299(1097):483-95. doi: 10.1098/rstb.1982.0146.
A selective survey of the literature reveals at least three major anion-dependent cation transport systems, defined as Na+ + Cl-, K+ + Cl- and Na+ + K+ + Cl- respectively. In human red cells, kinetic data on the fraction of K+ and Na+ influx inhibitable by bumetanide are presented to indicate an Na+:K+ stoichiometry of 1:2. For LK sheep red cells the large Cl- -dependent K+ leak induced by swelling is shown to share many characteristics with that induced by N-ethylmaleimide (NEM) treatment. NEM has complex effects, both inhibiting and then activating Cl- -dependent K+ fluxes dependent on NEM concentration. The alloantibody anti-L can prevent the action of NEM. In human red cells NEM induces a large Cl- -dependent specific K+ flux, which shows saturation kinetics. Its anion preference is Cl- greater than Br- greater than SCN- greater than I- greater than NO3- greater than MeSO4-. This transport pathway is not inhibited by oligomycin or SITS, although phloretin and high concentrations of furosemide and bumetanide (over 0.3 mM) do inhibit. Quinine (0.5 mM) is also an inhibitor. It is concluded that at least two distinct Cl- -dependent transport pathways for K+ are inducible in mammalian red cells, although the evidence for their separation is not absolute.
对文献的选择性调查显示至少有三种主要的阴离子依赖性阳离子转运系统,分别定义为Na⁺+Cl⁻、K⁺+Cl⁻和Na⁺+K⁺+Cl⁻。在人类红细胞中,给出了布美他尼可抑制的K⁺和Na⁺流入部分的动力学数据,以表明Na⁺:K⁺化学计量比为1:2。对于长寿命(LK)绵羊红细胞,肿胀诱导的大量Cl⁻依赖性K⁺泄漏显示出与N - 乙基马来酰亚胺(NEM)处理诱导的许多共同特征。NEM具有复杂的作用,根据NEM浓度,它先抑制然后激活Cl⁻依赖性K⁺通量。同种抗体抗 - L可阻止NEM的作用。在人类红细胞中,NEM诱导大量Cl⁻依赖性特异性K⁺通量,其呈现饱和动力学。其对阴离子的偏好顺序为Cl⁻>Br⁻>SCN⁻>I⁻>NO₃⁻>MeSO₄⁻。尽管根皮素以及高浓度的速尿和布美他尼(超过0.3 mM)确实有抑制作用,但该转运途径不受寡霉素或4 - 乙酰胺基 - 4'- 异硫氰酸基芪 - 2,2'- 二磺酸(SITS)抑制。奎宁(0.5 mM)也是一种抑制剂。得出的结论是,尽管哺乳动物红细胞中两种不同的Cl⁻依赖性K⁺转运途径的分离证据并不绝对,但至少这两种途径是可诱导的。