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Am J Physiol Cell Physiol 255: C808-C815, 1988;
0363-6143/88 $5.00
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AJP - Cell Physiology, Vol 255, Issue 6 C808-C815, Copyright © 1988 by American Physiological Society

ARTICLES

Apical membrane potassium conductance in guinea pig gallbladder epithelial cells

P. J. Gunter-Smith
Physiology Department, Armed Forces Radiobiology Research Institute, Bethesda, Maryland 20814-5145.

The fractional resistance of the apical membrane (fRa) of guinea pig gallbladder epithelial cells was observed to vary with changes in apical membrane potential (Va). Depolarizing Va from a base-line potential of -60 to -30 mV decreased fRa from 0.79 +/- 0.03 to 0.59 +/- 0.05. A comparable hyperpolarization had no effect on fRa. The potassium channel blocker tetraethylammonium (TEA) inhibited the changes in fRa induced by voltage when added to the mucosal but not when added to the serosal solution. Mucosal addition of Ba2+ and decreased pH also inhibited changes in fRa, whereas quinidine and 4-amino-pyridine did not. These results indicate that an increase in the K+ conductance of the apical membrane is responsible for changes in fRa with membrane depolarization. The current-voltage relation of this TEA-sensitive pathway was determined from differences in transepithelial current in the presence and absence of maximally effective concentrations of TEA and analyzed with respect to the Goldman constant-field equation. Computer-generated, best-fit analysis to the data indicated that they cannot be easily reconciled with K+ movement through a voltage-independent pathway or channel. Taken together, the results suggest that activation of a voltage-dependent K+ conductance in the apical membrane is responsible for changes in fRa with Va. This conductance also appears to be Ca2+-sensitive as ionomycin caused a shift in the relation between Va and fRa.


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