Jungwirth A, Paulmichl M, Lang F
Institute for Physiology, University of Innsbruck, Austria.
Biochim Biophys Acta. 1990 Sep 1;1054(2):143-8. doi: 10.1016/0167-4889(90)90234-5.
Cobalt has been shown to stimulate sodium transport across the distal nephron of the newt kidney. The mechanism of this action remained elusive. The present study has been performed to test for effects of cobalt on electrical properties of cultured subconfluent kidney (MDCK)-cells: cobalt (10 microM) leads to a rapid, sustained and reversible hyperpolarization of the cell membrane, paralleled by an increase of the potassium selectivity and a decrease of the resistance. Thus, cobalt increases the potassium conductance of the cell membrane. The half-maximal effect is elicited by approx. 1 microM. At extracellular calcium concentration reduced to less than 0.1 microM, cobalt (10 microM) leads to a transient hyperpolarization, which can be elicited only once. Thus, cobalt enhances the potassium conductance in a calcium dependent way. At higher concentrations (100 microM) cobalt hyperpolarizes the cell membrane only transiently even in the presence of extracellular calcium. Furthermore 100 microM cobalt interferes with ATP-induced hyperpolarization, which is known to result from calcium mediated activation of K+ channels. Thus, 100 microM cobalt may inhibit ATP-stimulated calcium entry into the cell.
钴已被证明能刺激蝾螈肾脏远端肾单位的钠转运。这种作用机制仍不清楚。本研究旨在测试钴对培养的亚汇合肾（MDCK）细胞电特性的影响：钴（10微摩尔）导致细胞膜快速、持续且可逆的超极化，同时钾选择性增加，电阻降低。因此，钴增加了细胞膜的钾电导。约1微摩尔可引发半数最大效应。在细胞外钙浓度降至低于0.1微摩尔时，钴（10微摩尔）导致短暂的超极化，且只能引发一次。因此，钴以钙依赖的方式增强钾电导。在较高浓度（100微摩尔）时，即使存在细胞外钙，钴也只会使细胞膜短暂超极化。此外，100微摩尔钴会干扰ATP诱导的超极化，已知这是由钙介导的钾通道激活所致。因此，100微摩尔钴可能会抑制ATP刺激的钙进入细胞。
