Wills N K
J Physiol. 1985 Jan;358:433-45. doi: 10.1113/jphysiol.1985.sp015560.
The apical membranes of surface cells in the rabbit descending colon possess a significant ionic conductance in parallel to amiloride-blockable Na+ channels. The identity of the ion(s) responsible for the amiloride-insensitive conductance is unknown. The purpose of the present paper was to assess the permeability and net driving forces for K+ and Cl- across this membrane using conventional and ion-sensitive micro-electrode techniques. Intracellular Cl- activity (aiCl) averaged 23 +/- 2 mM with an equilibrium potential (ECl) of -38 +/- 2 mV. This value is less than previous estimates of the electromotive force (e.m.f.) of the amiloride-insensitive pathway (ca. -50 mV). Consequently, Cl- alone cannot account for the amiloride-insensitive conductance. Replacement of Cl- by gluconate in the serosal solution decreased aiCl to 17 +/- 2.8 mM. aiCl was lowered to approximately 1 mM by replacement in the mucosal bath or by replacement in both solutions. The results indicate a low Cl- conductance in the basolateral membrane, in agreement with previous electrophysiological studies of this epithelium. In contrast to Cl-, the chemical driving force for K+ was large enough to support the e.m.f. of the amiloride-insensitive pathway (K+ equilibrium potential, EK = -66 mV). The basolateral membrane potential (Vbl), EK and the intracellular K+ activity (aiK) were decreased in parallel following inhibition of the basolateral Na-K pump, providing evidence that Vbl is largely due to a K+ diffusion potential. In the presence of serosal 10(-4) M-ouabain, aiK appeared to remain above equilibrium and more than doubled after addition of Ba2+ to the serosal bath. Replacement of the mucosal bathing solution with KCl or gluconate Ringer solution largely restored Vbl and the transepithelial potential (VT) in tissues which had been previously treated with ouabain. The restoration of VT was decreased and the transepithelial resistance (RT) was increased by addition of tetraethylammonium to the mucosal bath. The above results suggest that there are at least four routes for ion movement across the apical membrane of rabbit colon surface epithelial cells. These are: (1) an amiloride-sensitive Na+ channel, (2) a K+ conductance, (3) electroneutral uptake of Cl- from lumen to cell interior and (4) an active K+ transport mechanism, also from lumen to cell interior.
兔降结肠表面细胞的顶端膜具有与氨氯地平可阻断的Na⁺通道平行的显著离子电导。对氨氯地平不敏感电导负责的离子身份尚不清楚。本文的目的是使用传统和离子敏感微电极技术评估K⁺和Cl⁻跨该膜的通透性和净驱动力。细胞内Cl⁻活性(aiCl)平均为23±2 mM,平衡电位(ECl)为-38±2 mV。该值小于先前对氨氯地平不敏感途径的电动势(e.m.f.)的估计值(约-50 mV)。因此,仅Cl⁻不能解释氨氯地平不敏感电导。在浆膜溶液中用葡萄糖酸盐替代Cl⁻可使aiCl降至17±2.8 mM。通过在黏膜浴中替代或在两种溶液中替代,aiCl降至约1 mM。结果表明基底外侧膜中Cl⁻电导较低,这与先前对该上皮的电生理研究一致。与Cl⁻相反,K⁺的化学驱动力足以支持氨氯地平不敏感途径的电动势(K⁺平衡电位,EK = -66 mV)。在抑制基底外侧Na-K泵后,基底外侧膜电位(Vbl)、EK和细胞内K⁺活性(aiK)平行下降,这表明Vbl很大程度上归因于K⁺扩散电位。在存在浆膜10⁻⁴ M哇巴因的情况下,aiK似乎保持在平衡以上,并且在向浆膜浴中添加Ba²⁺后增加了一倍多。用KCl或葡萄糖酸盐林格溶液替代黏膜浴溶液在很大程度上恢复了先前用哇巴因处理过的组织中的Vbl和跨上皮电位(VT)。通过向黏膜浴中添加四乙铵,VT的恢复降低,跨上皮电阻(RT)增加。上述结果表明,至少有四条离子跨兔结肠表面上皮细胞顶端膜移动的途径。这些途径是:(1)氨氯地平敏感的Na⁺通道,(2)K⁺电导,(3)从管腔到细胞内部的Cl⁻电中性摄取,以及(4)一种也从管腔到细胞内部的主动K⁺转运机制。