Active K+ absorption by the gastric mucosa: inhibition by omeprazole.

Unidirectional fluxes of K+ across the histamine-stimulated frog gastric mucosa bathed in Cl(-)-Ringer were measured. Comparison of nutrient-to-secretory and secretory-to-nutrient K+ fluxes determined using either 42K or 86Rb as radioisotopic tracers gave identical results, and thus either isotope could be used for K+ flux measurements; the majority of these experiments used 86Rb as the tracer. Short-circuited mucosas maintained a small net absorption of 0.07 +/- 0.03 mueq X cm-2 X h-1 (n = 9). Omeprazole decreased acid secretion from 4.98 +/- 0.58 to 0.08 +/- 0.02 mueq X cm-2 X h-1 and reversed the direction of net K+ flux giving a net secretion of 0.09 +/- 0.04 mueq X cm-2 X h-1. Ouabain increased the rate of K+ absorption to 0.32 +/- 0.08 mueq X cm-2 X h-1 with a flux ratio (JKn----s/JKs----n) of 0.31 +/- 0.09; subsequent addition of omeprazole significantly decreased the rate of K+ absorption and increased the flux ratio. Omeprazole did not alter the fraction of transmucosal current carried by either K+ or Cl-. For omeprazole inhibited-mucosas at open circuit increasing the secretory osmolarity by 100 mosM with sucrose decreased the transmucosal resistance by 14% and increased nutrient-to-secretory K+ flux by 31%. For actively secreting mucosas no significant changes were seen in either parameter. These results are shown to be consistent with an electroneutral apical H+-K+ exchange pump and diffusion from the gland lumen-to-the secretory fluid, being rate limiting for K+ flux.