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Am J Physiol Gastrointest Liver Physiol 279: G400-G410, 2000;
0193-1857/00 $5.00
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Vol. 279, Issue 2, G400-G410, August 2000

NH4Cl inhibition of acid secretion: possible involvement of an apical K+ channel in bullfrog oxyntic cells

Susan J. Hagen, Hui Wu, and Sarah W. Morrison

Department of Surgery, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215

This study was undertaken to determine the mechanism by which ammonium chloride (NH4Cl) inhibits stimulated acid secretion in the bullfrog gastric mucosa. To this end, four possible pathways of inhibition were studied: 1) blockade of basolateral K+ channel, 2) blockade of ion transport activity, 3) neutralization of secreted H+ in the luminal solution, or 4) ATP depletion. Addition of nutrient 10 mM NH4Cl (calculated NH3 concentration = 92.5 µM and NH4+ concentration = 9.91 mM) inhibited acid secretion within 30 min. Inhibition of acid secretion did not occur by blockade of basolateral K+ channel activity or ion transport activity or by neutralization of the luminal solution. Although ATP depletion occurred in the presence of NH4Cl, the magnitude of ATP depletion in 30 min was not sufficient to inhibit stimulated acid secretion. By comparing the effect of NH4Cl on the resistance of inhibited or stimulated tissues, we demonstrate that NH4Cl acts specifically on stimulated tissues. We propose that NH4Cl blocks activity of an apical K+ channel present in stimulated oxyntic cells. Our data suggest that the activity of this channel is important for the regulation of acid secretion in bullfrog oxyntic cells.

Rana catesbeiana; gastric mucosa; ammonia


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