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

This study was undertaken to determine the mechanism by which ammonium chlo ride (NH4Cl) inhibits stimulated acid secretion in the bullfrog gastric muc osa. To this end, four possible pathways of inhibition were studied: 1) blo ckade 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 mu M and NH4+ concentration = 9.91 mM) inhibited acid secretion within 30 min. Inhibition of acid secretion did not occur by blockade of basolateral K+ ch annel activity or ion transport activity or by neutralization of the lumina l solution. Although ATP depletion occurred in the presence of NH4Cl, the m agnitude of ATP depletion in 30 min was not sufficient to inhibit stimulate d acid secretion. By comparing the effect of NH4Cl on the resistance of inh ibited or stimulated tissues, we demonstrate that NH4Cl acts specifically o n stimulated tissues. We propose that NH4Cl blocks activity of an apical K channel present in stimulated oxyntic cells. Our data suggest that the act ivity of this channel is important for the regulation of acid secretion in bullfrog oxyntic cells.