Post M A, Dawson D C
Department of Physiology, University of Michigan Medical School, Ann Arbor 48109.
Am J Physiol. 1992 Apr;262(4 Pt 1):C1089-94. doi: 10.1152/ajpcell.1992.262.4.C1089.
An amiloride-inhibitable, Na(+)-H+ antiporter was identified in the basolateral membrane of turtle colon by measuring 22Na+ fluxes across isolated tissues apically permeabilized with the pore-forming antibiotic amphotericin B. In cells shrunken by exposure to Cl(-)-free (gluconate) solutions and treated with ouabain to block the Na-K-ATPase, Na+ movement across the basolateral membrane was due entirely to the antiporter. Elevation of cytosolic Na+ was associated with an amiloride-inhibitable outward current across the basolateral membrane. The sensitivity of the current to various amiloride analogues paralleled that of Na+ exchange rather than that of the apical Na+ channel. Furthermore, cell volume changes altered basolateral Na+ exchange and basolateral Na+ conductance in a parallel fashion. We propose that this amiloride-sensitive basolateral Na+ conductance represents an altered operating mode of a basolateral Na(+)-H+ exchanger.
通过测量经成孔抗生素两性霉素B使顶端通透的离体组织上的22Na+通量，在龟结肠的基底外侧膜中鉴定出一种氨氯吡脒可抑制的Na(+)-H+逆向转运体。在暴露于无Cl(-)（葡萄糖酸盐）溶液而收缩并用哇巴因处理以阻断Na-K-ATP酶的细胞中，Na+跨基底外侧膜的移动完全归因于该逆向转运体。胞质Na+升高与氨氯吡脒可抑制的跨基底外侧膜外向电流相关。该电流对各种氨氯吡脒类似物的敏感性与Na+交换而非顶端Na+通道的敏感性平行。此外，细胞体积变化以平行方式改变基底外侧Na+交换和基底外侧Na+电导。我们提出这种对氨氯吡脒敏感的基底外侧Na+电导代表了基底外侧Na(+)-H+交换体的一种改变的运作模式。
