Sidium-dependent ion cotransport in steady-state Ehrlich ascites tumor cells
- 1 June 1985
- journal article
- research article
- Published by Springer Nature in The Journal of Membrane Biology
- Vol. 87 (2) , 121-130
- https://doi.org/10.1007/bf01870658
Abstract
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 150mm Na+ 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 20mm Na+ and is maintained up to 55mm. Thus, over the range 1 to 55mm Na+ 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 150mm Na+, 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 150mm Na+ 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+].This publication has 28 references indexed in Scilit:
- Self‐inhibition of chloride transport in ehrlich ascites tumor cellsJournal of Cellular Physiology, 1984
- Thiol-Dependent passive K/Cl transport in sheep red cells: IV. Furosemide inhibition as a function of external Rb+, Na+, and Cl−The Journal of Membrane Biology, 1984
- Volume-induced increase of K+ and Cl− permeabilities in Ehrlich ascites tumor cells. Role of internal Ca2+The Journal of Membrane Biology, 1984
- Na+, Cl− cotransport in Ehrlich ascites tumor cells activated during volume regulation (regulatory volume increase)The Journal of Membrane Biology, 1983
- Volume-induced increase of anion permeability in human lymphocytes.The Journal of general physiology, 1982
- Osmoregulatory Salt Transporting Mechanisms: Control of Cell Volume in Anisotonic MediaAnnual Review of Physiology, 1981
- K+ influx components in ascites cells: The effects of agents interacting with the (Na++K+)-pumpThe Journal of Membrane Biology, 1980
- Chloride and sulfate transport in ehrlich ascites tumor cells: Evidence for a common mechanismJournal of Cellular Physiology, 1978
- Chloride self exchange in Ehrlich ascites cells. Inhibition by furosemide and 4-acetamido-4′-isothiocyanostilbene-2-2′-disulfonic acidBiochimica et Biophysica Acta (BBA) - Biomembranes, 1977
- Cation permeability and ouabain-insensitive cation flux in the Ehrlich ascites tumor cellThe Journal of Membrane Biology, 1975