Calcium, cell shrinkage, and prolytic state of human red blood cells
Autor: | Jeffrey C. Freedman, L. M. Crespo, T. S. Novak |
---|---|
Rok vydání: | 1987 |
Předmět: |
Adult
Cell Membrane Permeability Erythrocytes Physiology Membrane Fluidity Sodium Ionophore chemistry.chemical_element Calcium Hemolysis Calcium in biology Membrane Potentials Valinomycin chemistry.chemical_compound Membrane Lipids Chlorides medicine Humans Vanadate Egtazic Acid Calcimycin Chemistry Erythrocyte Membrane Electric Conductivity Biological Transport Cell Biology Membrane transport Red blood cell medicine.anatomical_structure Biochemistry Biophysics Potassium |
Zdroj: | The American journal of physiology. 252(2 Pt 1) |
ISSN: | 0002-9513 |
Popis: | The effects of intracellular calcium, or Cac, on the Na permeability of human red blood cells were examined during 3-h incubations with the Ca ionophore A23187 and varied external Ca, Cao. Above 3 microM Cao, Nac increased significantly as ATP decreased. Maintenance of normal ATP with vanadate did not prevent the gain of Nac. Similar amounts of Nac were gained in 3 h by ouabain-treated cells exposed to the K ionophore valinomycin or by cells osmotically shrunken. Cells shrunken with sucrose also exhibited partial loss of Kc. When the cells with increased Nac were subsequently transferred to Na-free, high-K medium, the Nac and Kc that had changed slowly over 3 h returned toward normal within 10 min. The development of irreversible high cation permeability in shrunken cells was not prevented by a variety of transport inhibitors. These observations and cell volume distributions suggest that prolonged shrinkage induces a subpopulation of cells to become highly cation permeable, or "prolytic". The major effect of Cac on Na permeability appears to be an indirect consequence of cell shrinkage due to KCl loss. |
Databáze: | OpenAIRE |
Externí odkaz: |