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钾离子对蛙视网膜色素上皮细胞牛磺酸转运的调节作用

Potassium modulation of taurine transport across the frog retinal pigment epithelium.

作者信息

Miller S S, Steinberg R H

出版信息

J Gen Physiol. 1979 Aug;74(2):237-59. doi: 10.1085/jgp.74.2.237.

Abstract

Net taurine transport across the frog retinal pigment epithelium-choroid was measured as a function of extracellular potassium concentration, [K+]o. The net rate of retina-to-choroid transport increased monotonically as [K+]o increased from 0.2 mM to 2 mM on the apical (neural retinal) side of the tissue. No further increase was observed when [k+]o was elevated to 5 mM. The [K+]o changes that modulate taurine transport approximate the light-induced [K+]o changes that occur in the extracellular space separating the photoreceptors and the apical membrane of the pigment epithelium. The taurine-potassium interaction was studied by using rubidium as a substitute for potassium and measuring active rubidium transport as a function of extracellular taurine concentration. An increase in apical taurine concentration, from 0.2 mM to 2 mM, produced a threefold increase in active rubidium transport, retina to choroid. Net taurine transport can also be altered by relatively large, 55 mM, changes in [Na+]o. Apical ouabain, 10(-4) M, inhibited active taurine, rubidium, and potassium transport; in the case of taurine, this inhibition is most likely due to a decrease in the sodium electrochemical gradient. In sum, these results suggest that the apical membrane contains a taurine, sodium co-transport mechanism whose rate is modulated, indirectly, through the sodium pump. This pump has previously been shown to be electrogenic and located on the apical membrane, and its rate is modulated, indirectly, by the taurine co-transport mechanism.

摘要

测量了牛磺酸跨青蛙视网膜色素上皮-脉络膜的净转运情况,并将其作为细胞外钾离子浓度[K⁺]ₒ的函数。当组织顶端(神经视网膜)一侧的[K⁺]ₒ从0.2 mM增加到2 mM时,视网膜到脉络膜的净转运速率单调增加。当[K⁺]ₒ升高到5 mM时,未观察到进一步增加。调节牛磺酸转运的[K⁺]ₒ变化近似于在分隔光感受器和色素上皮顶端膜的细胞外空间中发生的光诱导[K⁺]ₒ变化。通过使用铷替代钾并测量主动铷转运作为细胞外牛磺酸浓度的函数来研究牛磺酸-钾相互作用。顶端牛磺酸浓度从0.2 mM增加到2 mM,使视网膜到脉络膜的主动铷转运增加了三倍。相对较大的55 mM的[Na⁺]ₒ变化也可改变牛磺酸的净转运。顶端施加10⁻⁴ M的哇巴因可抑制牛磺酸、铷和钾的主动转运;就牛磺酸而言,这种抑制很可能是由于钠电化学梯度降低所致。总之,这些结果表明顶端膜含有一种牛磺酸-钠共转运机制,其速率通过钠泵间接调节。先前已证明该泵是生电的且位于顶端膜上,其速率通过牛磺酸共转运机制间接调节。

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