Inhibition of gastric mucosal carbonic anhydrase by taurocholic acid and other ulcerogenic agents.
Carbonic anhydrase, an enzyme catalyzing hydration of CO2 and vice versa, is exceptionally abundant in the gastric mucosa, including the surface epithelial cells where it seems to have a protective function. The present study evaluated various ulcerogenic agents in terms of their ability to influence the activity of carbonic anhydrase in the gastric mucosa. Taurocholic acid, acetylsalicylic acid, and ethanol all significantly inhibited carbonic anhydrase derived from gastric mucosa of the rat in in vitro conditions, and this inhibition occurred in concentrations that are likely to be present within the stomach. In contrast, lysolecithin and urea had no effect on carbonic anhydrase activity. In in vivo situations, intragastric taurocholic acid (20 mM) likewise significantly inhibited the activity of carbonic anhydrase in the gastric mucosa. The inhibition was stronger in the presence of luminal acid (hydrochloric acid, 100 mM) than in the absence of it. In contrast, intragastric acetylsalicylic acid (20 mM) or ethanol (20 percent vol/vol) had no effect. Yet, intravenous acetylsalicylic acid (20 mg/kg body weight) did have a slight but significant inhibitory action. The results indicate that taurocholic acid is able to inhibit gastric mucosal carbonic anhydrase, a feature which may contribute to its ulcerogenic action. Even though acetylsalicylic acid and ethanol likewise inhibit gastric carbonic anhydrase in vitro conditions, their action in in vivo situations remains questionable.
D000818:Animals; D001241:Aspirin / Q000494:pharmacology; D002257:Carbonic Anhydrase Inhibitors; D002256:Carbonic Anhydrases; D005753:Gastric Mucosa / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains; D013656:Taurocholic Acid / Q000494:pharmacology
D002257:Carbonic Anhydrase Inhibitors; D013656:Taurocholic Acid; D002256:Carbonic Anhydrases; D001241:Aspirin