Davis C W, Finn A L
Fed Proc. 1985 Jun;44(9):2520-5.
We have studied the problem of cell volume homeostasis in toad and frog urinary bladder by using electrophysiological measurements and an optical measure of cell volume. After osmotically induced swelling, urinary bladder cells spontaneously regulate their volume through a net loss of potassium, chloride, and water. During inhibition of sodium transport by amiloride the cells swell to the same extent as controls, but the volume-regulatory process is blocked. Electrophysiological results under isosmotic conditions indicate that basolateral membrane resistance increases simultaneously with the amiloride-induced rise in apical membrane resistance during transport inhibition. These independent observations indicate that inhibition of apical membrane sodium entry results in a secondary decrease in basolateral membrane potassium permeability. When cells are exposed to calcium-free, hyposmotic Ringer's solution, cell volume regulation is blocked; subsequent addition of the calcium ionophore A23187 is ineffective in restoring the regulatory process. The ionophore does induce volume regulation, however, in amiloride-inhibited, osmotically swollen cells in the presence of external calcium. Calcium thus seems to control basolateral membrane potassium permeability and may be the intracellular mediator of apical and basolateral membrane interactions.
我们通过电生理测量和细胞体积的光学测量方法，研究了蟾蜍和青蛙膀胱中细胞体积稳态的问题。在渗透性肿胀后，膀胱细胞通过钾、氯和水的净流失自发调节其体积。在氨氯地平抑制钠转运期间，细胞肿胀程度与对照组相同，但体积调节过程被阻断。等渗条件下的电生理结果表明，在转运抑制期间，基底外侧膜电阻增加，同时氨氯地平诱导顶端膜电阻升高。这些独立的观察结果表明，顶端膜钠内流的抑制导致基底外侧膜钾通透性继发性降低。当细胞暴露于无钙、低渗的林格氏液中时，细胞体积调节被阻断；随后添加钙离子载体A23187无法恢复调节过程。然而，在外部钙存在的情况下，该离子载体确实能诱导氨氯地平抑制的、渗透性肿胀细胞的体积调节。因此，钙似乎控制着基底外侧膜钾通透性，并且可能是顶端膜和基底外侧膜相互作用的细胞内介质。
