Schwab A, Oberleithner H
Institut für Physiologie, Universität Würzburg, Federal Republic of Germany.
Pflugers Arch. 1988 Mar;411(3):268-72. doi: 10.1007/BF00585113.
In frog diluting segment transepithelial K+ net flux (JKte) occurs via trans- and paracellular transport routes. Inhibition of transcellular K+ transport discloses JKte across the shunt-pathway. By means of K+-sensitive microelectrodes we have measured secretory JKte induced by an acute K+ load, in the diluting segment of the isolated and doubly-perfused frog kidney. Transcellular K+ transport was inhibited by blocking the luminal K+ permeability either directly by barium or indirectly by the diuretic drug amiloride (via intracellular acidification induced by inhibition of Na+/H+ exchange), by the Na+/K+ pump inhibitor ouabain or by inducing an acute acid load. All experimental maneouvers led to a reduction of secretory JKte to about 50% of the control JKte. The apparent permeability coefficient for K+ of this nephron portion after inhibition of transcellular secretory JKte was reduced to a similar extent. We conclude: In frog diluting segment the ratio of trans- over paracellular JKte is close to unity. This ratio represents a minimum estimate because inhibition of the transcellular K+ pathway by barium, amiloride or an acute acid load may have been incomplete. Acidosis and/or amiloride exert large antikaliuretic effects due to the inhibition of the luminal K+ permeability.
在蛙类稀释段,跨上皮钾离子净通量(JKte)通过跨细胞和细胞旁转运途径发生。跨细胞钾离子转运的抑制揭示了通过旁路途径的JKte。借助钾离子敏感微电极,我们在分离并双灌注的蛙肾稀释段中测量了急性钾负荷诱导的分泌性JKte。通过钡直接阻断管腔钾离子通透性、通过利尿药氨氯吡脒间接阻断(通过抑制钠/氢交换诱导细胞内酸化)、通过钠/钾泵抑制剂哇巴因或通过诱导急性酸负荷来抑制跨细胞钾离子转运。所有实验操作均导致分泌性JKte降低至对照JKte的约50%。跨细胞分泌性JKte被抑制后,该肾单位部分钾离子的表观通透系数也降低到类似程度。我们得出结论:在蛙类稀释段,跨细胞与细胞旁JKte的比例接近1。该比例是一个最低估计值,因为钡、氨氯吡脒或急性酸负荷对跨细胞钾离子途径的抑制可能并不完全。酸中毒和/或氨氯吡脒由于抑制管腔钾离子通透性而发挥强大的抗利尿作用。