INDUCTION OF A CA2+-ACTIVATED K+ CHANNEL IN HUMAN ERYTHROCYTES BY MECHANICAL-STRESS

Mechanical deformation of normal ATP-replete human erythrocytes increased their permeability to Ca2+ sufficiently to turn on the Ca2+-activated K+ channel (the Gardos channel). When Ca2+ is absent, mechanical deformation of normal erythrocytes induces an equivalent increase the permeability of both Na+ and K+, In the presence of 0.1 to 1 mM Ca2+, a further increase in the K+ efflux rate was seen. There was no increase in Na+ flux above that induced by deformation itself. The involvement of the Ca2+-activated H channel was verified by showing the specific inhibitors of the channel, quinine and charybdotoxin, prevent the Ca2+-induced increase in K+ efflux. These results are consistent with a model of sickle cell dehydration proposed by Bookchin et al. ((1987) Prog. Clin. Biol. Res. 240, 193-200). The estimated rate of Ca2+ entry under these conditions (37-degrees-C, 1000 dyne/cm2, and laminar shear) was about 1 mmol/loc per h.