Characterization of increased K+ permeability associated with the stimulation of receptors for immunoglobulin E on rat basophilic leukemia cells.

Abstract

Aggregation of immunoglobulin E-receptor complexes on the surface of rat basophilic leukemia cells stimulates an increase in plasma membrane K+ permeability that is monitored as an increase in the rate of efflux of preloaded 86Rb+. A major component of this stimulated 86Rb+ efflux appears to be due to a Ca(2+)-activated K+ channel because it is inhibited by quinidine in parallel with the inhibition of degranulation and membrane potential repolarization, it is blocked by 0.1 mM La3+, and it is dependent on external Ca2+. Depolarization of the plasma membrane by carbonyl cyanide 3-chlorophenylhydrazone inhibits stimulated Ca2+ influx and prevents antigen-induced 86Rb+ efflux, and increased external Ca2+ partially restores 86Rb+ efflux under these conditions. In addition, potentiation of antigen-stimulated Ca2+ influx by pretreatment with cholera toxin increases the initial rate of stimulated 86Rb+ efflux. Another component of antigen-stimulated K+ efflux appears to be mediated by a guanine nucleotide-binding protein because pretreatment of rat basophilic leukemia cells with pertussis toxin decreases the initial rate of antigen-stimulated 86Rb+ efflux to 40% of that for the untreated cells. Stimulated 86Rb+ efflux is also observed when ionomycin is used to increase cytoplasmic Ca2+ and to trigger membrane depolarization. The efflux stimulated by ionomycin is inhibited by quinidine but not by pertussis toxin pretreatment; thus, it appears to occur through the Ca(2+)-activated K+ efflux pathway. It is proposed that these K+ efflux pathways serve to sustain the Ca2+ influx that is necessary for receptor-mediated triggering of cellular degranulation.

• Authors: G F Labrecque, D Holowka, B Baird
• Journal: The Journal of biological chemistry (J Biol Chem) Vol. 266 Issue 23 Pg. 14912-7 (Aug 15 1991) ISSN: 0021-9258 [Print] United States
• PMID: 1831198 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S., Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Antigens, Differentiation, B-Lymphocyte
• Receptors, Fc
• Receptors, IgE
• Virulence Factors, Bordetella
• Colforsin
• Immunoglobulin E
• Carbonyl Cyanide m-Chlorophenyl Hydrazone
• Ionomycin
• Cholera Toxin
• Pertussis Toxin
• Quinidine
• Rubidium
• Potassium

Topics

• Animals
• Antigens, Differentiation, B-Lymphocyte (metabolism)
• Basophils (metabolism)
• Biological Transport (drug effects)
• Carbonyl Cyanide m-Chlorophenyl Hydrazone (pharmacology)
• Cell Membrane Permeability (drug effects)
• Cholera Toxin (pharmacology)
• Colforsin (pharmacology)
• Immunoglobulin E (metabolism)
• Ionomycin (pharmacology)
• Leukemia, Experimental
• Pertussis Toxin
• Potassium (metabolism)
• Quinidine (pharmacology)
• Rats
• Receptors, Fc (metabolism)
• Receptors, IgE
• Rubidium (metabolism)
• Tumor Cells, Cultured
• Virulence Factors, Bordetella (pharmacology)