Electrophysiological effects of mucosal Cl- removal in Necturus gallbladder epithelium.
The factors responsible for the cell membrane hyperpolarization elicited in Necturus gallbladder epithelium on Cl- removal from the mucosal bathing solution were evaluated with conventional and ion-sensitive microelectrode techniques. Cl- removal causes reversal of apical Cl- -HCO3- exchange, resulting in a fall in intracellular Cl- activity (aiCl) and an increase in intracellular pH (pHi). Concomitantly, the cell membranes hyperpolarize to values close to the K+ equilibrium potential (EK), aiNa falls, and aiK rises. The observed changes in membrane voltage are not attributable to a pHi-dependent increase in cell membrane K+ permeability (PK), because 1) the cell membrane resistances increased and 2) elevating solution partial pressure of CO2 (PCO2) to counterbalance the cellular alkalinization on mucosal Cl- removal caused a further hyperpolarization of the cell membranes to values greater than EK. This additional hyperpolarization was related to the activity of the Na+ pump, inasmuch as it was accompanied by an increase in aiNa and was ouabain sensitive. These results are consistent with, but do not prove, pump electrogenicity. During the period of Cl- removal from the mucosal bathing solution, the cell membrane depolarization caused by raising serosal K+ concentration was increased, whereas the depolarization caused by lowering serosal Cl- concentration was decreased, compared with substitutions under control conditions. These results indicate that mucosal Cl- removal causes a decrease in basolateral PCl, which we speculate could be due to a decrease in cell volume. We conclude that the hyperpolarization of the cell membranes on mucosal Cl- removal is primarily due to the combined effects of the fall in basolateral PCl and the increase in basolateral ECl.
Stoddard
J S
JS
Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston, Texas 77550.
Reuss
L
L
D000818:Animals; D001692:Biological Transport; D001784:Blood Gas Analysis; D002245:Carbon Dioxide / Q000097:blood / Q000494:pharmacology; D002462:Cell Membrane / Q000378:metabolism / Q000502:physiology; D002712:Chlorides / Q000378:metabolism*; D004553:Electric Conductivity; D004594:Electrophysiology; D004847:Epithelial Cells; D004848:Epithelium / Q000378:metabolism / Q000502:physiology; D005704:Gallbladder / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D006863:Hydrogen-Ion Concentration; D008564:Membrane Potentials / Q000187:drug effects; D009092:Mucous Membrane / Q000166:cytology / Q000378:metabolism / Q000502:physiology; D009337:Necturus / Q000502:physiology*; D010042:Ouabain / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism / Q000502:physiology
D002712:Chlorides; D002245:Carbon Dioxide; D010042:Ouabain; D012964:Sodium