AJP - Cell Physiology, Vol 263, Issue 5 C917-C932, Copyright © 1992 by American Physiological Society
Erythrocyte K-Cl cotransport: properties and regulation
P. K. Lauf, J. Bauer, N. C. Adragna, H. Fujise, A. M. Zade-Oppen, K. H. Ryu and E. Delpire
Department of Physiology and Biophysics, Wright State University, Dayton, Ohio 45401-0927.
Erythrocytes possess a Cl-dependent, Na-independent K transport system
cotransporting K and Cl in a 1:1 stoichiometry that is membrane potential
independent. This K-Cl cotransporter is stimulated by cell swelling,
acidification, Mg depletion, and thiol modification. Cell shrinkage,
elevation of cellular divalent ions, thiol alkylation, phosphatase
inhibitors, and derivatives of certain loop diuretics and stilbenes are
inhibitory. Thus regulation of K-Cl cotransport at the membrane and
cytoplasmic levels is highly complex. Basal K-Cl cotransport decreases with
cellular maturation, whereas its modes of stimulation and inhibition are
variable between species. The physiological inactivation appears to be
prevented in low-K animal erythrocytes. In certain human
hemoglobinopathies, K-Cl cotransport may be the cause of cellular
dehydration and volume decrease. K-Cl cotransport occurs also in
nonerythroid cells, such as in epithelial and liver cells of other species.
At the threshold of molecular characterization, this comprehensive review
places our present understanding of the mechanisms modulating K-Cl
cotransport physiologically and pathophysiologically into kinetic and
thermodynamic perspectives.
