AJP - Cell Physiology, Vol 259, Issue 5 C746-C751, Copyright © 1990 by American Physiological Society
Erythrocyte cation permeability induced by mechanical stress: a model for sickle cell cation loss
R. M. Johnson and S. A. Gannon
Department of Biochemistry, Wayne State Medical School, Detroit, Michigan 48201.
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.
