Induction of a Ca(2+)-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 Ca(2+)-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 Ca(2+)-activated H channel was verified by showing the specific inhibitors of the channel, quinine and charybdotoxin, prevent the Ca(2+)-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.
Johnson
R M
RM
Department of Biochemistry, Wayne State Medical School, Detroit, MI 48201.
Tang
K
K
D000255:Adenosine Triphosphate / Q000097:blood; D002118:Calcium / Q000494:pharmacology*; D004912:Erythrocytes / Q000502:physiology*; D006801:Humans; D066298:In Vitro Techniques; D011188:Potassium / Q000097:blood; D015221:Potassium Channels / Q000502:physiology*; D012964:Sodium / Q000097:blood; D013314:Stress, Mechanical
D015221:Potassium Channels; D000255:Adenosine Triphosphate; D012964:Sodium; D011188:Potassium; D002118:Calcium