Erythrocyte cation permeability induced by mechanical stress: a model for sickle cell cation loss.
Human red blood cells were subjected to mechanical shearing in a Couette viscometer at 37 degrees C, using polyvinylpyrrolidone to increase the medium viscosity. At stresses greater than 300 dyn/cm2, movement of both Na and K down their concentration gradients was observed. The net rate of both monovalent cation fluxes appeared to be linear with applied stress in the range of 300-910 dyn/cm2. The applied shear forces caused no fragmentation of the cells. Observed hemolysis was slight. The observed cation fluxes are not a result of hemolysis because the amount of K released by the hemolyzed cells is quantitatively inadequate to account for the net K efflux, and there is a net uptake of Na by the stressed erythrocytes, which cannot be a consequence of hemolysis. The rates of net Na uptake and K efflux were nearly equal (ratio = 0.93 +/- 0.40, n = 6). The stress-induced permeabilities were reversible when shearing was halted. This work demonstrates the existence of cation permeability inducible in the red cell membrane by mechanical deformation, which may be a model for the sickling-induced monovalent cation exchange observed in deoxygenated sickle cells.
Johnson
R M
RM
Department of Biochemistry, Wayne State Medical School, Detroit, Michigan 48201.
Gannon
S A
SA
D000755:Anemia, Sickle Cell / Q000097:blood*; D002412:Cations; D002463:Cell Membrane Permeability; D004910:Erythrocyte Membrane / Q000502:physiology*; D004912:Erythrocytes / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007700:Kinetics; D008954:Models, Biological; D011188:Potassium / Q000097:blood; D012964:Sodium / Q000097:blood; D013314:Stress, Mechanical
D002412:Cations; D012964:Sodium; D011188:Potassium