Effects of H+ and HCO3- secretion on mucus gel pH in isolated antral mucosa of bullfrog stomach.

To study the mechanism of self-protection of the gastric surface epithelium, we measured the pH gradient of the mucus gel layer in the isolated bullfrog antral mucosa with pH-sensitive microelectrodes in the Ussing chamber preparation. Under the control condition of 15mM HCO3- and 1.5% CO2 serosal perfusion, the pH on the interface between luminal solution and mucus gel layer (pHLMI) was 6.04 +/- 0.12 (n = 7), and the pH on the interface between the mucus gel layer and epithelial cell (pHMEI) was 5.69 +/- 0.13 (n = 7). When gastric acid secretion was stimulated by histamine (10(-4) M), the pHLMI became 5.43 +/- 0.12 (n = 4) and the pHMEI 4.40 +/- 0.18 (n = 4). Inhibition of acid secretion by cimetidine (10(-4) M) raised the pHLMI to 6.51 +/- 0.07 (n = 7) and the pHMEI to 6.23 +/- 0.08 (n = 7). Omeprazole (10(-4) M) also raised the pHLMI and the pHMEI to 6.78 +/- 0.13 (n = 7) and 6.56 +/- 0.13 (n = 7), respectively. These data suggested that the H+ ions secreted from the oxyntic cells were able to diffuse to the lateral side within the mucus gel layer, affecting the local pH just above the surface epithelial cells. Under high serosal HCO3- condition (45mM HCO3- and 1.5% CO2 in serosal side), the pHLMI and the pHMEI were elevated to 7.22 +/- 0.10 (n = 7) and 6.92 +/- 0.10 (n = 7), respectively. This result suggested that HCO3- secretion, which was served to neutralize the invading acid, depended upon the supply of HCO3- from the serosal medium. Thus, the serosal HCO3- would be working not only in the acid-protection, but also in the maintenance of pH gradient across the mucus gel layer.