Cell volume and metabolic dependence of NEM-activated K+-Cl- flux in human red blood cells.

The effects of incubation in anisosmotic media and of metabolic depletion on ouabain-resistant (OR) Cl--dependent K+ influxes stimulated by N-ethylmaleimide (NEM) were studied in human red blood cells using Rb+ as K+ analogue. The NEM-stimulated but not the basal Rb+-Cl- influx measured in phosphate-buffered anisosmotic media was found to be cell volume dependent. When cellular ATP, [ATP]c, was lowered to less than 0.10 of its initial level by exposure to nonmetabolizable 2-deoxy-D-glucose, the NEM-stimulated but not the basal Cl--dependent Rb+ influxes were abolished. Metabolically depleted red blood cells subsequently repleted by incubation in glucose plus inosine regained the NEM-inducible Rb+ (K+) transport activity. The difference in the time course of ATP breakdown and Rb+ influx inhibition suggests that energization of the NEM-stimulated Rb+ flux by metabolism may involve factors additional to ATP.

[1]  H. D. Kim,et al.  Pig reticulocytes. V. Development of Rb+ influx during in vitro maturation , 1984, Journal of cellular physiology.

[2]  A. Cossins,et al.  Sodium and potassium transport in trout (Salmo gairdneri) erythrocytes. , 1984, The Journal of physiology.

[3]  C. Anderson,et al.  Passive potassium transport in LK sheep red cells. Modification by N- ethyl maleimide , 1983, The Journal of general physiology.

[4]  D. Tosteson,et al.  Red Cell Lithium‐Sodium Countertransport and Sodium‐Potassium Cotransport in Patients with Essential Hypertension , 1982, Hypertension.

[5]  P. Weber,et al.  Sodium‐Lithium Exchange and Sodium‐Potassium Cotransport in Human Erythrocytes: Part 2: A Simple Uptake Test Applied to Normotensive and Essential Hypertensive Individuals , 1982, Hypertension.

[6]  J. Ciccone,et al.  Inhibition of the Na+/K+ cotransport system by cyclic AMP and intracellular Ca2+ in human red cells. , 1982, Biochimica et biophysica acta.

[7]  M. Saier,et al.  (Na+,K+)-cotransport in the Madin-Darby canine kidney cell line. Kinetic characterization of the interaction between Na+ and K+. , 1982, The Journal of biological chemistry.

[8]  A. Distler,et al.  Abnormal Sodium Efflux in Erythrocytes of Patients with Essential Hypertension , 1982, Hypertension.

[9]  M. McNamee,et al.  Activation and inactivation kinetics of Torpedo californica acetylcholine receptor in reconstituted membranes. , 1982, Biochemistry.

[10]  T. Thien,et al.  Cation Fluxes and Na+‐K+‐Activated ATPase Activity in Erythrocytes of Patients with Essential Hypertension , 1981, Hypertension.

[11]  P. Dunham,et al.  Passive potassium transport in low potassium sheep red cells: dependence upon cell volume and chloride. , 1981, The Journal of physiology.

[12]  M. Devynck,et al.  Inherited defect in a Na+, K+ -co-transport system in erythrocytes from essential hypertensive patients , 1980, Nature.

[13]  P. Lauf,et al.  A chloride dependent K+ flux induced by N-ethylmaleimide in genetically low K+ sheep and goat erythrocytes. , 1980, Biochemical and biophysical research communications.

[14]  P. Cala.  Volume regulation by flounder red blood cells in anisotonic media , 1977, The Journal of general physiology.

[15]  R. A. Cooper,et al.  A furosemide-sensitive cotransport of sodium plus potassium in the human red cell. , 1974, The Journal of clinical investigation.

[16]  F. Kregenow.  The Response of Duck Erythrocytes to Nonhemolytic Hypotonic Media , 1971, The Journal of general physiology.

[17]  N. Adragna,et al.  The Kinetics of Ouabain Inhibition and the Partition of Rubidium Influx in Human Red Blood Cells , 1971, The Journal of general physiology.

[18]  K. Fugelli.  Regulation of cell volume in flounder (Pleuronectes flesus) erythrocytes accompanying a decrease in plasma osmolarity. , 1967, Comparative biochemistry and physiology.

[19]  O. H. Lowry,et al.  EFFECT OF ISCHEMIA ON KNOWN SUBSTRATES AND COFACTORS OF THE GLYCOLYTIC PATHWAY IN BRAIN. , 1964, The Journal of biological chemistry.