Frindt G, Lee C O, Yang J M, Windhager E E
Department of Physiology, Cornell University Medical College, New York, N.Y.
Miner Electrolyte Metab. 1988;14(1):40-7.
Experimental maneuvers that increase intracellular calcium ion levels inhibit sodium transport by renal tubules. In the isolated perfused renal tubule, intracellular calcium ion activity (aiCa) changes in response to alterations in the magnitude of the electrochemical potential gradient for sodium ions across the basolateral cell membrane. However, a potassium-induced depolarization of this cell boundary does not cause a rise but rather a fall in intracellular calcium ion levels. Ionomycin raises aiCa without causing intracellular acidification. This observation does not support the view that high cytosolic calcium produces intracellular acidification. At least in the case of ionomycin, the inhibition of sodium transport appears to be due to ionophore-induced increases in aiCa. The changes in intracellular calcium ion concentration found in the different experimental conditions studied were consistent with the notion that cytosolic calcium ions may mediate a feedback mechanism that links the luminal entry to the peritubular extrusion of sodium ions. The mechanisms by which cytosolic calcium alters entry is not yet clear but recent experiments suggest an indirect effect on sodium channel activity.
增加细胞内钙离子水平的实验操作会抑制肾小管的钠转运。在离体灌注的肾小管中，细胞内钙离子活性（aiCa）会随着钠离子跨基底外侧细胞膜电化学势梯度大小的改变而变化。然而，钾离子诱导的这种细胞边界去极化并不会导致细胞内钙离子水平升高，反而会使其降低。离子霉素可提高aiCa而不引起细胞内酸化。这一观察结果不支持高细胞质钙会导致细胞内酸化的观点。至少在离子霉素的情况下，钠转运的抑制似乎是由于离子载体诱导的aiCa增加。在所研究的不同实验条件下发现的细胞内钙离子浓度变化与以下观点一致，即细胞质钙离子可能介导一种反馈机制，该机制将管腔进入与钠离子的肾小管周围排出联系起来。细胞质钙改变进入的机制尚不清楚，但最近的实验表明其对钠通道活性有间接影响。
