AJP - Cell Physiology, Vol 258, Issue 6 C1016-C1024, Copyright © 1990 by American Physiological Society
Mechanisms underlying volume regulatory decrease by Necturus gallbladder epithelium
T. J. Furlong and K. R. Spring
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892.
Volume regulatory decrease (VRD) by Necturus gallbladder epithelial cells
in Cl Ringer was unaffected by the addition of 5 mM BaCl2 to apical
perfusates but was inhibited by the addition of 5 mM BaCl2 and 50 or 3
microM phencyclidine (PCP) to serosal perfusates, suggesting that K
channels in the basolateral membrane were activated during VRD. VRD was
unaffected by replacement of Cl with NO3 or SCN, suggesting that
Cl-dependent Na-K-Cl and K-Cl cotransport were not involved. In SCN Ringer,
VRD was inhibited by the addition of 0.1 mM bumetanide to serosal
perfusates, suggesting that bumetanide-sensitive anion channels in the
basolateral membrane were also activated. A transient 10-mV
hyperpolarization of the membrane potential was associated with VRD. The
channel blockers that inhibited VRD had little or no effect on the
hyperpolarization, suggesting that the changes in membrane potential were
unrelated to the changes in cell volume. Perfusion of the apical surface of
the epithelium with isotonic solutions containing 10 mM D-glucose resulted
in a variable increase in cell volume followed by a variable shrinkage to
normal, suggesting that VRD was also activated during organic solute
absorption. The increase in cell volume was blocked by the addition of 0.01
or 1 mM phlorizin to mucosal perfusates. The reduction in cell volume was
inhibited by the addition of 0.1 mM bumetanide, but not BaCl2 or PCP, to
serosal perfusates, indicating the the shrinkage mechanism secondary to
glucose addition differed from that seen after exposure to hypotonic
perfusates.
