Sodium-dependent ion cotransport in steady-state Ehrlich ascites tumor cells.
Sodium-dependent ion cotransport in steady-state Ehrlich ascites tumor cells.
复制标题
稳态艾利希腹水肿瘤细胞中钠依赖性离子共转运。
DOI:
10.1007/bf01870658
复制
发表时间:
1985
期刊:
影响因子:
--
通讯作者:
Levinson,C
中科院分区:
文献类型:
--
作者:
Levinson,C
The Ehrlich tumor cell possesses and anion-cation cotransport system which operates as a bidirectional exchanger during the physiological steady state. This cotransport system, like that associated with the volume regulatory mechanism (i.e. coupled net uptake of Cl−+Na+and/or K+) is Cl−-selective and furosemide-sensitive, suggesting the same mechanism operating in two different modes. Since Na+has an important function in the volume regulatory response, its role in steady-state cotransport was investigated. In the absence of Na+, ouabain-insensitive K+and DIDS-insensitive Cl−transport (KCl cotransport) are low and equivalent to that found in 150mmNa+medium containing furosemide. Increasing the [Na+] results in parallel increases in K+and Cl−transport. The maximum rate of each (18 to 20 meq/(kg dry wt)·min) is reached at about 20mmNa+and is maintained up to 55mm. Thus, over the range 1 to 55mmNa+the stoichiometry of KCl cotransport is 1∶1. In contrast to K+and Cl−, furosemide-sensitive Na+transport is undetectable until the [Na+] exceeds 50mm. From 50 to 150mmNa+, it progressively rises to 7 meq/(kg dry wt)·min, while K+and Cl−transport decrease to 9 and 16 meq/(kg dry wt)·min, respectively. Thus, at 150mmNa+the stoichiometric relationship between Cl−, Na+and K+is 2∶1∶1. These results are consistent with the proposal that the Cl−-dependent cation cotransport system when operating during the steady state mediates the exchange of KCl for KCl or NaCl for NaCl; the relative proportion of each determined by the extracellular [Na+].