Swelling-activated anion conductance in skate hepatocytes:
regulation by cell cl- and atp.
Jackson, Paul S., Kevin Churchwell, Nazzareno Ballatori, James L.
Boyer, and Kevin Strange.
Mount Desert Island Biological Laboratory, Salsbury Cove, ME and
Critical Care Research Laboratories, Children's Hospital, Boston, MA;
Departments of Medicine (Nephrology), Neurosurgery and
Anesthesiology, Children's Hospital and Harvard Medical School,
Boston, MA 02115; Department of Environmental Medicine, University of
Rochester School of Medicine, Rochester, NY 14642; Department of
Medicine and Liver Center, Yale University School of Medicine, New
Haven, CT 06510
APStracts 2:0259C, 1995.
Cell swelling activates an outwardly rectifying anion conductance in
mammalian cells. The channel responsible for this conductance
mediates volume regulatory efflux of organic osmolytes such as
taurine. We observed a similar conductance in hepatocytes from the
skate Raja erinacea. Whole cell Cl- conductance was increased
>100 fold by a 2 fold increase in hepatocyte volume. The
conductance was outwardly rectifying and had a relative cation
permeability of 0.2. Cation permeability was increased by reductions
in patch pipette CsCl concentration suggesting that the channel pore
contains saturable anion and cation binding sites with different
anion and cation affinities. The conductance had a broad anion
selectivity and a relative taurine permeability of 0.17. Activation
of the conductance required intracellular ATP or a nonhydrolyzable
ATP analog. Elevation of intracellular Cl- from 20-155 mM reduced
current activation while the rate and extent of cell swelling were
unaffected. Reduction of intracellular Cl- concentration to 5-10 mM
caused spontaneous current activation without cell swelling. These
results suggest that increases in cell Cl- levels increase the volume
set-point of the channel. We propose that the main function of the
outwardly rectifying anion channel is nonselective transport of
organic solutes.
Received 23 May 1995; accepted in final form 7 July 1995.
APS Manuscript Number C298-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 18 July 1995.