Effect of imidazoles on active transport by gastric mucosa and urinary bladder

Publisher Website
Google Scholar
Abstract
Studies were undertaken to determine whether the stimulatory effect of histamine and the methyl xanthines on the frog gastric mucosa in vitro could be ascribed to the imidazole component of these compounds. The actively transported ions of gastric secretion appear in the form of hydrochloric acid and of a nonacid chloride component that is responsible for the short-circuit current (Isc). At 10–2 m, imidazole reduced acid secretion (Jh) by 80%, which was somewhat greater than the reduction produced by thiocyanate. N-methylimidazole, 2-methylimidazole, 4(5)-methylimidazole, and benzimidazole abolished Jh. The Isc tended to rise as Jh fell. In stimulated mucosae, imidazole and N-methylimidazole promptly reduced oxygen consumption (qO2) by 25%; thiocyanate had a delayed and lesser effect. Pyrazole, 4-hydroxymethylimidazole, and tris had little or no effect on Jh, Isc, or qO2. Imidazole and N-methylimidazole reduced active sodium transport by the toad urinary bladder by 50%. The results indicate that the inhibitory effects of the imidazoles cannot be ascribed to their buffering capacity or to competitive inhibition of histamine. Instead the effects may result from depletion of tissue content of adenosine-3',5'-phosphate or from interference with protein-bound phosphohistidine in oxidative phosphorylation.