Showing papers by "Keiko Shiratori published in 1997"
TL;DR: Cysteamines-induced acid hypersecretion is mediated mainly by cysteamine-induced gastrin release and partially by cholinergic factors, which appears to be independent ofCholinergic tone.
Abstract: Cysteamine has been known to stimulate gastric acid secretion and to induce duodenal ulcers in rats. We investigated the role of gastrin in cysteamine-induced acid hypersecretion in the perfused rat stomach. Intravenous infusion of cysteamine (75 mg/kg/h) resulted in a significant increase in acid secretion, which was accompanied by a marked increase in the plasma gastrin concentration. The cysteamine-induced increase in gastric acid secretion was completely blocked by i.v. injection of anti-gastrin rabbit serum (500 μl). In addition, i.v. infusion of a CCK-B/ gastrin receptor antagonist (L-365,26()) (1 mg/kg/h) also suppressed the cysteamine-induced increase in acid secretion. Atropine significantly, but only partially, inhibited the increase. The elevated plasma gastrin levels induced by cysteamine were unaffected by atropine and L-365,260. In conclusion, cysteamine-induced acid hypersecretion is mediated mainly by cysteamine-induced gastrin release and partially by cholinergic factors. Furthermore, gastrin release caused by cysteamine appears to be independent of cholinergic tone.
4 citations
Journal Article•
TL;DR: Investigation of the effect of intraduodenal amino acids on gastric acid secretion and gastrin release in rats indicates that intestinal AA regulate gastric secretory function mediated by AA-released endogenous secretin in the intestinal phase.
Abstract: We investigated the effect of intraduodenal amino acids (AA) on gastric acid secretion and gastrin release, and possible role of endogenous secretin on this phenomenon in vivo in rats. Intraduodenal administration of mixed AA solution (140 mg/hr, pH6.5) resulted in significant inhibition of gastric acid secretion and gastrin release stimulated by intragastric perfusion of peptone (0.5%). Intravenous infusion of secretin (0.05CU/kg/hr) also inhibited peptone-stimulated gastric acid secretion and gastrin release. Furthermore, the AA-induced suppression of gastric acid secretion was significantly blocked by intravenous injection of rabbit anti-secretin serum. In conclusion, intraduodenal AA inhibit peptone-stimulated gastric acid secretion and gastrin release, and endogenous secretin released by AA is attributed to this suppression. Thus, the result of this study indicates that intestinal AA regulate gastric secretory function mediated by AA-released endogenous secretin in the intestinal phase.
2 citations