Effects of acetylsalicylate on alkalinization, acid secretion and electrogenic properties in the isolated gastric mucosa.
The effects of acetylsalicylate (ASA) on the in vitro secretory and electrical properties of Necturus and Rana temporaria gastric mucosa have been studied. The gastric antrum alkalinized the luminal surface, while in the fundus it is likely that acidificaiton and alkalinization occur simultaneously and that net secretion is due to the dominance of one or other of these processes. The histamine H2  receptor antagonist Metiamide was used to inhibit acid secretion for studies on fundic alkalinization in Rana temporaria. Submucosal application of 3 mM ASA for 30 min markedly reduced alkalinization in the antrum and the frog fundus. Following removal of ASA there was only partial recovery of this secretion. The drug caused slight inhibtion of spontaneous acid secretion in Necturus fundus but not of histamine-stimulated acid secretion in the frog fundus. Following salicylate removal, the rate of acid secretion increased to a higher level than before administration in both tissues. There was a small flux of ASA across the mucosa which was greatest in the acid secreting frog fundus (4.38mumol cm-2 min-1) and least in the antrum (2.19 mumol cm-2 min-1). Esposure of the gastric mucosa to ASA was generally associated with a fall in transmucosal electric potential difference and short-circuit current together with an increase in electrical resistance. It is proposed that the greater sensitivity of alkalinization to ASA is responsible for the apparent increase in the rate of acid secretion which occured.
Effects of acetylsalicylate on alkalinization, acid secretion and electrogenic properties in the isolated gastric mucosa. The effects of acetylsalicylate (ASA) on the in vitro secretory and electrical properties of Necturus and Rana temporaria gastric mucosa have been studied. The gastric antrum alkalinized the luminal surface, while in the fundus it is likely that acidificaiton and alkalinization occur simultaneously and that net secretion is due to the dominance of one or other of these processes. The histamine H2  receptor antagonist Metiamide was used to inhibit acid secretion for studies on fundic alkalinization in Rana temporaria. Submucosal application of 3 mM ASA for 30 min markedly reduced alkalinization in the antrum and the frog fundus. Following removal of ASA there was only partial recovery of this secretion. The drug caused slight inhibtion of spontaneous acid secretion in Necturus fundus but not of histamine-stimulated acid secretion in the frog fundus. Following salicylate removal, the rate of acid secretion increased to a higher level than before administration in both tissues. There was a small flux of ASA across the mucosa which was greatest in the acid secreting frog fundus (4.38mumol cm-2 min-1) and least in the antrum (2.19 mumol cm-2 min-1). Esposure of the gastric mucosa to ASA was generally associated with a fall in transmucosal electric potential difference and short-circuit current together with an increase in electrical resistance. It is proposed that the greater sensitivity of alkalinization to ASA is responsible for the apparent increase in the rate of acid secretion which occured.