AJP - Cell Physiology, Vol 253, Issue 5 C693-C699, Copyright © 1987 by American Physiological Society
SITS-sensitive Cl- conductance pathway in chick intestinal cells
M. Montrose, J. Randles and G. A. Kimmich
Department of Radiation Biology and Biophysics, School of Medicine and Dentistry, University of Rochester, New York 14642.
The unidirectional influx of 36Cl- into isolated chick epithelial cells is
30% inhibited by 300 microM SITS. Characteristics of the SITS-sensitive
flux pathway were examined in terms of sensitivity to changes in membrane
potential and intracellular pH. Potential dependence was evaluated using
unidirectional influx of [14C]tetraphenylphosphonium ([14C]-TPP+) as a
qualitative sensor of diffusion potentials created by experimentally
imposed gradients of Cl-. Steady-state distribution of [14C]methylamine
([14C]MA) was used to examine for Cl(-)-dependent changes in intracellular
pH. Imposed Na+ gradients, but not Cl- gradients, induce changes in [14C]MA
distribution. SITS does not alter the [14C]MA distribution observed in
cells with imposed gradients of Na+ and Cl-. Both results suggest that
inhibition of Cl(-)-OH- exchange system is not the basis for the SITS
effect on Cl- influx. However, if relative permeabilities for ion pairs via
conductance pathways are compared, it can be shown that SITS causes a
marked reduction of Pcl relative to either PNa or PK. SITS also inhibits
electrically induced influx of [14C]TPP+ or [14C] alpha-methylglucoside
driven by imposed Cl- gradients. Conversely, electrically driven Cl- influx
can be blocked by SITS. These observations are all consistent with a
SITS-sensitive Cl- conductance pathway associated with the plasma membrane
of chick intestinal cells. No Cl(-)-OH- exchange capability can be detected
for chick intestinal cells.
