AJP - Cell Physiology, Vol 263, Issue 1 C187-C193, Copyright © 1992 by American Physiological Society
Regulation of apical membrane ion transport in Necturus gallbladder
J. L. Garvin and K. R. Spring
Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, Bethesda, Maryland 20892.
Na and Cl movement through the apical membrane of Necturus gallbladder
epithelium was investigated using electrophysiological and light
microscopic measurements. Changes in membrane potential difference,
fractional resistance of the apical membrane, and transepithelial
resistance caused by changes in apical bath Cl concentration revealed the
presence of a Cl conductance in the apical membrane of control tissues that
was apparently not present in the preparations studied by other
investigators. This Cl conductance was blocked by bumetanide (10(-5) M) or
by the inhibitor of adenosine 3',5'-cyclic monophosphate (cAMP) action, the
Rp isomer of adenosine 3',5'-cyclic monophosphorothioate (Rp-cAMPS; 0.5
mM). Treatment of the tissues with Rp-cAMPS also eliminated
bumetanide-sensitive cell swelling in the presence of ouabain and activated
an amiloride-sensitive swelling, changes consistent with inhibition of NaCl
cotransport and the activation of Na-H and Cl-HCO3 exchange. We conclude
that the mode of NaCl entry into Necturus gallbladder epithelial cells is
determined by the level of cAMP. When cAMP levels are high, entry occurs by
NaCl cotransport; when cAMP levels are low, parallel exchange of Na-H and
Cl-HCO3 predominates. These observations explain the previous disagreements
about the mode of NaCl entry into Necturus gallbladder epithelial cells.
