Gastric HCO3− secretion induced by mucosal acidification: Different mechanisms depending on acid concentration

Abstract

We compared the HCO3- secretory responses induced by mucosal acidification at different HCl concentrations (100 and 200 mM HCl) in the rat stomach. Under urethane anesthesia, the stomach was mounted on an ex vivo chamber and perfused with saline under inhibition of acid secretion by omeprazole (60 mg/kg, i.p.). TheHCO3- secretion was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. The acidification was performed by exposure of the mucosa to 100 mMor 200 mM HCl for 10 min. The secretion of HCO3- was increased by acidification of the mucosa at both 100 and 200 mM of HCl, and the maximal HCO3- response was 1.5-times greater at the latter concentration. The HCO3- responses induced by 100 and 200 mM HCl were both totally inhibited by prior administration of indomethacin, an inhibitor of prostaglandin (PG) production. The HCO3- stimulatory effect of 200 mM HCl was also significantly attenuated by pre-treatment with N(G)-nitro L-arginine methyl ester (L-NAME), the inhibitor of nitric oxide (NO) synthase, as well as chemical ablation of capsaicin-sensitive afferent neurons, whereas that of 100 mM HCl was affected by neither of these treatments. We conclude that the mucosal acidification stimulates gastric HCO3- secretion in different mechanisms, depending on the concentration of acid; the response caused by 100 mM HCl is mediated only by PGs, while that caused by 200 mM HCl is mediated by both capsaicin-sensitive afferent neurons and NO, in addition to PGs.

The Gastrointestinal Circulation: Physiology and Pathophysiology

“…The threshold pH required to compromise epithelial integrity (increased permeability to small solutes) is lower for the stomach (pH ≈ 0.8-1.0; 100-150 mmol/L HCl) (481) than the duodenum (pH ≈ 2.0; 10 mmol/L HCl) (357). A mucosal hyperemia, as well as an increased HCO 3 − secretion, is noted at or near the respective pH thresholds in both the stomach (3,4,481) and the duodenum (6,7).…”

Role for Ion Transport in Porcine Vocal Fold Epithelial Defense to Acid Challenge

“…5–7 HCO 3 − secretion in the stomach is mediated by multiple factors, including endogenous prostaglandins, nitric oxide, and neural pathways. 5,6 Our data suggest that vocal fold epithelia also secrete bicarbonate in response to acidic challenge. The molecular and neuronal pathways regulating HCO 3 − secretion in the vocal folds remain to be investigated.…”

“…Exposure to acid immediately increases HCO 3 − secretion in esophageal and gastric epithelia. 5-7 HCO 3 − secretion in the stomach is mediated by multiple factors, including endogenous prostaglandins, nitric oxide, and neural pathways. 5,6 Our data suggest that vocal fold epithelia also secrete bicarbonate in response to acidic challenge.…”

“…This study seeks to test the hypothesis that bicarbonate (HCO 3 − ) ion secretion could function as one such defense mechanism. In the epithelium of the esophagus and stomach, HCO 3 − is rapidly secreted in response to acid exposure 5 – 7 . HCO 3 − functions to neutralize acid, 8 and its secretion may help protect gastric and esophageal epithelia from acid‐induced injury.…”

“…In the epithelium of the esophagus and stomach, HCO 3 2 is rapidly secreted in response to acid exposure. [5][6][7] HCO 3 2 functions to neutralize acid, 8 and its secretion may help protect gastric and esophageal epithelia from acid-induced injury. Active ion transport contributes to the health and viability of the vocal fold epithelium.…”