Effect of carbenoxolone on alkaline secretion by isolated amphibian gastric and duodenal mucosa

Abstract

The influence of carbenoxolone sodium on HCO₃ transport has been examined in spontaneously alkalinizing amphibian antral (Necturus and Rana catesbeiana) and proximal duodenal (Rana cates‐beiana) mucosa and in cimetidine‐treated fundic mucosa (Rana temporario) in vitro. Low concentrations of carbenoxolone (10^‐6‐10^‐4 mol/1, serosal side and 10^‐5 mol/1, luminal side) did not affect the secretory rate or electrical properties of these tissues. In the stomach a higher concentration of carbenoxolone (10 ^‐3 mol/1, serosal side) caused an immediate fall in transmucosal potential difference (PD) and electrical resistance. There was an initial decrease in the rate of HCO₃ transport followed by an increase in titra‐table alkalinization due to passive permeation of base from the serosal bathing solution. The non‐steroidal anti‐inflammatory agent ibuprofen (3 times 10^‐3 mol/1, serosal side) inhibited alkaline secretion while the bile salt sodium taurocholate (10 ^‐4 mol/1, luminal side) converted net alkaline secretion to a titratable acidity in cimetidine‐treated fundus. Pretreatment of the mucosa with carbenoxolone (10^‐4 mol/1) did not influence the response to taurocholate but when added with ibuprofen, it potentiated the inhibitory effect of this drug on fundic alkaline secretion. In contrast, prostaglandin E₂ (10^‐6 mol/1) markedly reduced the inhibition of fundic alkaline secretion caused by ibuprofen. The anti‐ulcer properties of carbenoxolone do not appear to be related to effects on gastro‐duodenal HCO₃ transport.