Role of acid-base status in the response of the isolated amphibian gastric mucosa to back diffusion of H+.

The effect of a period of induced back diffusion of H+ on the isolated amphibian gastric mucosa was studied under various conditions. Under standard conditions (HCO3--buffered nutrient solution; 95% O2-5% CO2), passage of an electrical current of 500 microA/cm2 for 15 min from a secretory fluid of pH 2.10 across the mucosal resulted in a decrease of the transmucosal potential difference (PD) of 10.9 +/- 1.9 mV, a decrease of resistance (R) of 48 +/- 26 ogema cm2 and a decrease of short circuit current (Isc) of 18 +/- 7 microA/cm2. Flux of the neutral molecule, erythritol from secretory (S) to nutrient (N) fluid increased by 66% and the active transport of Cl- N lead to S decreased from 2.9 to 1.9 microeq/cm2/hr. With removal of HCO3- from the nutrient fluid and with inhibition of carbonic anhydrase activity the period of back diffusion induced significantly greater change in the electrical measurements than occurred when under standard conditions. This increased effect of back diffusion of H+ was not changed by change of the nutrient fluid pH from 7.20 to either 6.6 or 8.2. Increase of the HCO3- concentration of the nutrient fluid to 35 mM or decrease of the CO2 content of the aerating gas to 1% were associated with significantly less change of the electrical measurements than occurred with standard conditions. These studies support the proposal that the the neutralizing reaction HCO3- + H+ leads to CO2 + H2O plays a central role in the gastric mucosal handling of backing diffusing H+ and suggests that the capacity and poise of the HCO3-/CO2 buffer system is an important determinant of the ability of the mucosa to tolerate luminal acidity.