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首页> 外文期刊>The Journal of Physiology >Novel activation stimulus of chloride channels by potassium in human osteoblasts and human leukaemic T lymphocytes.
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Novel activation stimulus of chloride channels by potassium in human osteoblasts and human leukaemic T lymphocytes.

机译:人成骨细胞和人白血病T淋巴细胞中钾对氯离子通道的新型激活刺激。

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1. The whole-cell recording mode of the patch-clamp technique was used to study the effect of extracellular K+ and Rb+ on membrane currents in human osteoblasts, in a human osteoblast-like cell line, and in the Jurkat human leukaemic T cell line. 2. Increasing the extracellular concentration of K+ increased the membrane conductance of the cells in a concentration-dependent manner. This increase in membrane conductance was due to the activation of a Cl- conductance. Rb+ also induced this conductance, but conductance was less than half that seen in K+. 3. The Cl- channel blockers 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) and 4-acetamido-4'-isothiocyanatostilbene 2,2'-disulphonic acid (SITS) blocked the K(+)-induced Cl- current in a voltage-dependent manner. The degree of blockade increased with membrane depolarization to a maximum level at 40 mV. At potentials above this value the block appeared to decrease. 4. Both tonicity and K+ were required for maximal activation of the Cl- conductance since the K(+)-induced Cl- conductance could be inhibited by hypertonic solutions and the activation of a volume-sensitive Cl- conductance by hypotonic solutions could be enhanced by extracellular K+. 5. We conclude that an outwardly rectifying Cl- conductance can be activated either upon osmotic swelling or by an increase in extracellular K+. Both activation pathways may be involved in cell volume regulation and seem to apply to volume-sensitive Cl- channels in general since we observe this phenomenon in two different cell types, in human osteoblasts as well as in human leukaemic T lymphocytes.
机译:1.使用膜片钳技术的全细胞记录模式来研究细胞外K +和Rb +对人成骨细胞,人成骨细胞样细胞系和Jurkat人白血病T细胞系中膜电流的影响。 2.增加细胞外K +浓度以浓度依赖性方式增加细胞的膜电导。膜电导的增加是由于Cl-电导的激活。 Rb +也诱导了这种电导,但是电导小于在K +中看到的电导的一半。 3. Cl通道阻滞剂4,4'-二异硫氰基二苯乙烯-2,2'-二磺酸(DIDS)和4-乙酰氨基-4'-异硫氰基二苯乙烯2,2'-二磺酸(SITS)阻断了K(+)-以电压相关的方式感应Cl电流。阻滞程度随着膜的去极化作用增加到40 mV时的最大值。在高于该值的电势下,阻滞似乎减少。 4.高渗溶液可抑制K(+)诱导的Cl-电导,而高渗溶液可增强体积敏感性Cl-电导的活化,因此需要最大程度激活Cl-电导的张力和K +。通过细胞外K +。 5.我们得出结论,渗透性溶胀或细胞外K +升高均可激活向外整流的Cl-电导。这两种激活途径都可能参与细胞体积调节,并且似乎通常适用于体积敏感的Cl-通道,因为我们在人类成骨细胞和人类白血病T淋巴细胞的两种不同细胞类型中观察到了这种现象。

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