Nikiforov A A
Tsitologiia. 1985 Aug;27(8):887-94.
The stimulatory effect of cadmium ions on the Na-dependent fluorescein transport into the frog renal proximal tubules ceased with decreasing Ca++ concentration in solution on both the sides of the cell layer down to micromolar level. The decrease in Ca++ concentration per se stimulated fluorescein uptake during short-term incubations. A further diminution of Ca++ concentration in the tubular lumen with the aid of EGTA resulted in a sharp inhibition of the organic acid transport. Amiloride, which prevented the stimulatory effect of cadmium, inhibited the fluorescein transport at both millimolar and micromolar levels of Ca++ concentration, but it failed to affect the transport process after introducing EGTA into the tubular lumen. The results are discussed within the frames of a model regarding extracellular Ca++ as an allosteric inhibitor, and intracellular Ca++ as an allosteric activator of sodium channels in the apical membrane. Cd++ is assumed to compete with Ca++ for binding to centers of the allosteric inhibition, thereby accelerating the sodium ion flux across the cells of the proximal tubules.
随着细胞层两侧溶液中钙离子浓度降至微摩尔水平，镉离子对蛙肾近端小管中钠依赖性荧光素转运的刺激作用消失。在短期孵育过程中，钙离子浓度本身的降低会刺激荧光素摄取。借助乙二醇双（2-氨基乙基醚）四乙酸（EGTA）进一步降低肾小管腔中的钙离子浓度，会导致有机酸转运受到强烈抑制。氨氯吡咪可阻止镉的刺激作用，在毫摩尔和微摩尔水平的钙离子浓度下均抑制荧光素转运，但在将EGTA引入肾小管腔后，它未能影响转运过程。在将细胞外钙离子视为变构抑制剂、细胞内钙离子视为顶端膜中钠通道变构激活剂的模型框架内讨论了这些结果。假定镉离子与钙离子竞争结合变构抑制中心，从而加速钠离子通过近端小管细胞的通量。
