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Specific drug sensitive transport pathways for chloride and potassium ions in steady-state Ehrlich mouse ascites tumor cells.

Authors
  • Aull, F
Type
Published Article
Journal
Biochimica et Biophysica Acta
Publisher
Elsevier
Publication Date
Jun 28, 1982
Volume
688
Issue
3
Pages
740–746
Identifiers
PMID: 7115702
Source
Medline
License
Unknown

Abstract

A major aim of this investigation was to determine whether, in steady-state ascites cells, Cl- transport can be partitioned into a furosemide-sensitive cotransport with K+ and a separate 4,4'-isothiocyanostilbene-2,2'-disulfonic acid (DIDS) sensitive self-exchange. Both Cl- and K+ fluxes were studied. The furosemide- and Cl- sensitive K+ fluxes were equivalent, both in normal ionic media and when the external K+ concentration, [K+]o, was varied from 4 to 30 mM. The stoichiometry of the furosemide-sensitive Cl- and K+ fluxes was 2 Cl-:1 K+ at 0.1 and 0.5 mM drug levels but increased to 3 Cl-:1 K+ at 1.0 mM furosemide. DIDS at 0.1 mM had no effect on the K+ exchange rate but inhibited Cl- exchange by 39% +/- 2 (S.E.). The effects of DIDS and 0.5 mM furosemide on Cl- transport were additive but 1.0 mM furosemide and DIDS had overlapping inhibitory actions. Thus furosemide acts on components of K+ and Cl- transport which are linked to each other, but the drug also inhibits an additional DIDS-sensitive Cl- pathway, when present at higher concentrations. The dependence of the furosemide-sensitive K+ and Cl- transport on [K+]o was also studied; both fluxes fell as the [K+]o increased. The latter results recall those in an earlier study by Hempling (Hempling, H.G. (1962) J. Cell. Comp. Physiol. 60, 181-198).

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