Mechanisms of active Cl- secretion by frog gastric mucosa.

Net Cl- flux across the bullfrog gastric mucosa was examined to test the hypothesis that Cl-secretion (JClnet) can be driven by either of the two cation exchange pumps in the oxyntic cell. The effects on JClnet of ouabain, an Na+-K+ pump inhibitor, and omeprazole, an H+-K+ pump inhibitor were examined. Omeprazole abolished acid secretion (JH) and reduced JClnet in bullfrog gastric mucosa. For mucosae at open circuit the omeprazole-induced decrease in JH was not significantly different than the decrease in JClnet, and the transmucosal potential difference (PD) was increased. When short-circuited mucosae were treated with omeprazole, the decrease in JClnet was significantly less than the decrease in JH, and short-circuit current (SCC) was correspondingly increased. After treatment of short-circuited mucosae with ouabain, the omeprazole-induced decreases in JH and JClnet were not significantly different, and no change in SCC occurred. For open-circuited mucosae, pretreatment with ouabain resulted in a significantly smaller omeprazole-induced increase in the transmucosal PD than was seen without ouabain pretreatment. Our data 1) show that both the H+-K+ pump and the Na+-K+ pump can drive Cl- secretion and 2) suggest that inhibition of the H+-K+ pump with omeprazole stimulates the Na+-K+ pump.