RESISTANCE TO OSMOTIC LYSIS IN BXD-31 MOUSE ERYTHROCYTES - ASSOCIATION WITH UP-REGULATED K-CL COTRANSPORT

The decreased osmotic fragility and reduced K+ content of BXD-31 mouse erythrocytes arise from variation at a single genetic locus. We compa red ion transport in erythrocytes from BXD-31 mice and the parental st rain, DBA/2J. The strains had similar rates for Na-K pump, Na/H exchan ge, Na-K-2Cl cotransport, Ca2+-activated K+ channel, or AE1-mediated S O4 transport. In contrast, K-Cl cotransport was twice as active in BXD -31 as in DBA/2J cells. Cl--dependent K+ efflux from BXD-31 cells disp layed steep activation by acid pH (with maximal transport occurring at pH 6.75), whereas DBA/2J erythrocytes displayed a far less dramatic r esponse to pH. Both strains displayed regulatory volume decrease in re sponse to cell swelling. However, a 62% greater loss of cell K+ via K- Cl cotransport was observed in the BDX-31 strain. Furthermore the decr eased osmotic fragility of BXD-31 red blood cells was normalized by tr eatment with nystatin to achieve normal cell K+ and water content. Thu s upregulated K-Cl cotransport induces cell dehydration and K+ deficit in BXD-31 erythrocytes and causes their characteristic resistance to osmotic lysis.