Resistance to osmotic lysis in bxd-31 mouse erythrocytes:
association with upregulated k-cl cotransport .
Armsby, Carrie C., Alan K. Stuart-Tilley, Seth L. Alper, and Carlo
Brugnara.
Department of Laboratory Medicine, The ChildrenOs Hospital;
Molecular Medicine and Renal Units, Beth Israel Hospital; and
Departments of Pathology, Cell Biology, and Medicine, Harvard Medical
School, Boston, MA
APStracts 2:0367C, 1995.
The decreased osmotic fragility and reduced K+ content of BXD-31 mouse
erythrocytes arise from variation at a single genetic locus. We
compared ion transport in erythrocytes from BXD-31 mice and from the
parental strain, DBA/2J. The strains had similar rates for Na-K pump,
Na-H exchange, Na-K-2Cl cotransport, Ca2+-activated K+ channel, or
AE1-mediated SO4 transport. In contrast, K-Cl cotransport in BXD-31
cells was 2-fold more active than in DBA/2J cells. Cl-dependent K+
efflux from BXD-31 cells displayed steep activation by acid pH (with
maximal transport occurring at pH 6.75), whereas DBA-2J erythrocytes
displayed a far less dramatic response to pH. Both strains displayed
regulatory volume decrease (RVD) in response to cell swelling.
However, a 62% greater loss of cell K via K-Cl cotransport was
observed in BDX-31. Furthermore, the decreased osmotic fragility of
BXD-31 red cells was normalized by treatment with nystatin to achieve
normal cell K+ and water content. Thus, upregulated K-Cl cotransport
induces cell dehydration and K+ deficit in BXD-31 erythrocytes and
causes their characteristic resistance to osmotic lysis.
Received 29 June 1995; accepted in final form 15 September 1995.
APS Manuscript Number C392-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95