ELECTRICALLY SILENT COTRANSPORT OF NA+, K+ AND CL- IN EHRLICH CELLS
ELECTRICALLY SILENT COTRANSPORT OF NA+, K+ AND CL- IN EHRLICH CELLS
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DOI：
10.1016/0005-2736(80)90446-0
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发表时间：
1980-01-01
期刊：
影响因子：
--
通讯作者：
HEINZ, E
中科院分区：
文献类型：
--
作者：
GECK, P;PIETRZYK, C;HEINZ, E
本文描述了埃利希细胞中Na+、K+和Cl-的共转运系统。它对哇巴因不敏感，但在不影响相关离子其他途径的浓度下，可被呋塞米和其他高上限利尿剂特异性抑制。由于这些离子的呋塞米敏感通量不受膜电位变化的影响，并且由于呋塞米对其的完全抑制不会明显改变膜电位，因此它们似乎是电沉默的。脉冲响应方法在不可逆热力学方面的应用揭示了Na+、K+和Cl-（所有3种组合的q接近于1）在1：1：2的化学计量比下的呋塞米敏感流之间的紧密耦合。每种离子的位置似乎是相当具体的：K+可以被Rb+取代，但不能被测试的其他阳离子取代，而Cl-可以被Br-很差地取代，但不能被NO3-取代，与Cl--OH-交换系统相反。共转运系统似乎在细胞体积调节中起作用，因为它倾向于使细胞膨胀，从而抵消哇巴因敏感性（Na+，K+）泵的收缩效应。虽然运输和共轭驱动力之间的不一致性似乎表明主要的主动运输，这是非常不可能的，ATP的水解供应能量的运输过程中，因为没有刺激ATP营业额下观察到的cotransport系统的操作。
A cotransport system for Na+, K+ and Cl- in Ehrlich cells is described. It is insensitive towards ouabain, but specifically inhibited by furosemide and other high ceiling diuretics at concentrations which do not affect other pathways of the ions concerned. As the furosemide-sensitive fluxes of these ions are not affected by changes in membrane potential, and as their complete inhibition by furosemide does not appreciably alter the membrane potential, they appear to be electrically silent. Application of the pulse-response methods in terms of irreversible thermodynamics reveals tight coupling between the furosemide-sensitive flows of Na+, K+ and Cl- (q close to unity for all 3 combinations) at a stoichiometry of 1:1:2. The site for each of the ions appears to be rather specific: K+ can be replaced by Rb+, but not by other cations tested whereas Cl- can be poorly replaced by Br-, but not by NO3-, in contrast to the Cl--OH- exchange system. The cotransport system appears to function in cell volume regulation as it tends to make the cell swell, thus counteracting the shrinking effect of the ouabain-sensitive (Na+, K+) pump. While incongruence between transport and conjugated driving force seems to indicate primary active transport, it is very unlikely that hydrolysis of ATP supplies energy for the transport process, since there is no stimulation of ATP turnover observable under operation of the cotransport system.