Hebert S C, Friedman P A, Andreoli T E
J Membr Biol. 1984;80(3):201-19. doi: 10.1007/BF01868439.
This paper reports experiments designed to assess the relations between net salt absorption and transcellular routes for ion conductance in single mouse medullary thick ascending limbs of Henle microperfused in vitro. The experimental data indicate that ADH significantly increased the transepithelial electrical conductance, and that this conductance increase could be rationalized in terms of transcellular conductance changes. A minimal estimate (Gminc) of the transcellular conductance, estimated from Ba++ blockade of apical membrane K+ channels, indicated that Gminc was approximately 30-40% of the measured transepithelial conductance. In apical membranes, K+ was the major conductive species; and ADH increased the magnitude of a Ba++-sensitive K+ conductance under conditions where net Cl- absorption was nearly abolished. In basolateral membranes, ADH increased the magnitude of a Cl- conductance; this ADH-dependent increase in basal Cl- conductance depended on a simultaneous hormone-dependent increase in the rate of the net Cl- absorption. Cl- removal from luminal solutions had no detectable effect on Ge, and net Cl- absorption was reduced at luminal K+ concentrations less than 5mM; thus apical Cl- entry may have been a Na+, K+, 2Cl- cotransport process having a negligible conductance. The net rate of K+ secretion was approximately 10% of the net rate of Cl- absorption, while the chemical rate of net Cl- absorption was virtually equal to the equivalent short-circuit current. Thus net Cl- absorption was rheogenic; and approximately half of net Na+ absorption could be rationalized in terms of dissipative flux through the paracellular pathway. These findings, coupled with the observation that K+ was the principal conductive species in apical plasma membranes, support the view that the majority of K+ efflux from cell to lumen through the Ba++-sensitive apical K+ conductance pathway was recycled into cells by Na+, K+,2Cl- cotransport.
本文报道了旨在评估体外微灌流的单个小鼠髓袢升支粗段中净盐吸收与离子传导的跨细胞途径之间关系的实验。实验数据表明，抗利尿激素（ADH）显著增加了跨上皮电导，并且这种电导增加可以根据跨细胞电导变化来解释。从顶端膜钾通道的钡离子阻断估计的跨细胞电导的最小估计值（Gminc）表明，Gminc约为测得的跨上皮电导的30 - 40%。在顶端膜中，钾离子是主要的导电离子；并且在净氯离子吸收几乎被消除的条件下，ADH增加了钡离子敏感的钾离子电导的幅度。在基底外侧膜中，ADH增加了氯离子电导的幅度；这种依赖于ADH的基底氯离子电导增加取决于同时激素依赖的净氯离子吸收速率的增加。从管腔溶液中去除氯离子对Ge没有可检测到的影响，并且在管腔钾离子浓度低于5mM时净氯离子吸收减少；因此顶端氯离子进入可能是一种钠钾氯共转运过程，其电导可忽略不计。钾离子分泌的净速率约为氯离子吸收净速率的10%，而净氯离子吸收的化学速率实际上等于等效短路电流。因此净氯离子吸收是生电的；并且大约一半的净钠离子吸收可以根据通过细胞旁途径的耗散通量来解释。这些发现，再加上钾离子是顶端质膜中的主要导电离子这一观察结果，支持了这样一种观点，即通过钡离子敏感的顶端钾离子电导途径从细胞到管腔的大部分钾离子外流通过钠钾氯共转运被再循环回细胞中。
