Chloride transport in bullfrog gastric mucosa

Omeprazole uncouples histamine-stimulated hydrogen and chloride secretion in the frog gastric mucosa. This uncoupling results in a large increase in PD and Isc due to the unmasking of an electrogenic Cl- flux. Using a selective anoxia technique, we have attempted to define the cellular origin of this electrogenic Cl- flux. Sixteen bullfrog gastric mucosae were mounted in Ussing chambers. Under short-circuit conditions, PD, Isc, R, and unidirectional 36Cl flux were determined every 15 min. Acid secretion (10(-5) M histamine) was measured by hand titration (0.1 N NaOH). With both sides of the mucosae oxygenated, the addition of omeprazole (10(-4) M) resulted in cessation of H+ secretion and the unveiling of an electrogenic Cl- flux. Subsequent serosal anoxia (5% CO2-95% N2 nutrient side/30% O2 secretory side) resulted in a drop in JClnet associated with an appropriate fall in Isc. These changes were reversible with reoxygenation: (Table: see text). Bullfrog gastric mucosae which are partially oxygenated on the secretory side only (serosal anoxia) do not secrete acid in response to histamine. Therefore, the JClnet which is inhibited in these experiments by serosal anoxia may originate in the gastric glands approximately equal to 3.0 mu eq/cm2 X hr). The JClnet which remains during serosal anoxia may originate in the surface epithelial cells (approximately equal to 1.0 mu eq/cm2 X hr).