Beck J S, Breton S, Laprade R, Giebisch G
Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06510.
Am J Physiol. 1991 Jun;260(6 Pt 2):F861-7. doi: 10.1152/ajprenal.1991.260.6.F861.
The hypothesis that an increase of calcium leads to activation of calcium-activated ionic conductances during cell swelling was examined in the isolated perfused proximal convoluted tubule of the rabbit. Reduction of bath and luminal osmolality by 90 mosmol/kgH2O caused the cells to swell by 23.6 +/- 1.5% (n = 5) and intracellular calcium to rise from 227 +/- 35 to 347 +/- 60 nM (n = 6). Both these increases were transient, with volume decreasing to 5.5 +/- 1.2% above control and intracellular calcium concentration decreasing to 272 +/- 46 nM after 5-9 min. The addition of glucose and alanine to the tubule lumen to increase transcellular sodium transport caused a sustained increase in cell volume of 15.6 +/- 3.4% (n = 4). In parallel experiments, no significant increase in intracellular calcium concentration was observed. Addition of 1 microM of the calcium ionophore, ionomycin, reversibly increased intracellular calcium by 224 +/- 60 nM from a control value of 301 +/- 29 nM (n = 7) and reversibly depolarized the basolateral membrane by 3.6 +/- 0.9 mV (n = 5). However, there was no initial increase in the apparent transference number for potassium or chloride and no significant change in cell volume. We conclude from these observations that the sustained increase in basolateral potassium conductance observed when cells are swollen by hypotonicity or increased sodium transport (J. S. Beck and D. J. Potts. J. Physiol. Lond. 425: 369-378, 1990) is not due to a calcium-activated potassium conductance.
在兔离体灌注近端曲管中，研究了细胞肿胀期间钙增加导致钙激活离子电导激活的假说。将浴液和管腔渗透压降低90 mosmol/kgH₂O，使细胞肿胀23.6±1.5%（n = 5），细胞内钙从227±35 nM升至347±60 nM（n = 6）。这两种增加都是短暂的，5 - 9分钟后，体积降至比对照高5.5±1.2%，细胞内钙浓度降至272±46 nM。向肾小管腔添加葡萄糖和丙氨酸以增加跨细胞钠转运，导致细胞体积持续增加15.6±3.4%（n = 4）。在平行实验中，未观察到细胞内钙浓度有显著增加。添加1 μM钙离子载体离子霉素，使细胞内钙从对照值301±29 nM可逆地增加224±60 nM（n = 7），并使基底外侧膜可逆地去极化3.6±0.9 mV（n = 5）。然而，钾或氯的表观迁移数最初没有增加，细胞体积也没有显著变化。从这些观察结果我们得出结论，当细胞因低渗或钠转运增加而肿胀时观察到的基底外侧钾电导的持续增加（J. S. Beck和D. J. Potts. J. Physiol. Lond. 425: 369 - 378, 1990）不是由于钙激活钾电导。
