The role of carbonic anhydrase in gastric mucosal protection with special reference to H+ back diffusion and concomitant metabolic acidosis induced by acetazolamide.
It is suggested that carbonic anhydrase is implicated not only in gastric acid secretion, but in mucosal protection. It was reported that acetazolamide induced gastric mucosal lesions. But acetazolamide also caused concomitant metabolic acidosis by inhibiting H+ secretion from renal tubules. We investigated whether concomitant metabolic acidosis is implicated in gastric mucosal lesions induced by acetazolamide in vivo. We also evaluated the effect of acetazolamide on gastric H+ back diffusion in vivo. Correction of metabolic acidosis with sodium bicarbonate had no effect on the degree of the gastric mucosal lesions. Acetazolamide caused no change in gastric H+ and Na+ flux. These results suggest that metabolic acidosis induced by acetazolamide is not implicated in gastric mucosal lesions. Carbonic anhydrase has no effect on H+ back diffusion but may be implicated in mucosal protection by the disposition of back diffused H+ into the gastric mucosa.
D000086:Acetazolamide / Q000494:pharmacology*; D000138:Acidosis / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism*; D000818:Animals; D001639:Bicarbonates / Q000627:therapeutic use; D002256:Carbonic Anhydrases / Q000502:physiology*; D005753:Gastric Mucosa / Q000201:enzymology*; D006863:Hydrogen-Ion Concentration; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism / Q000627:therapeutic use; D017693:Sodium Bicarbonate; D013276:Stomach Ulcer / Q000139:chemically induced / Q000378:metabolism*
D001639:Bicarbonates; D017693:Sodium Bicarbonate; D012964:Sodium; D002256:Carbonic Anhydrases; D000086:Acetazolamide