BACKGROUND/AIMS: Evidence for gastrin-induced histamine secretion from isolated rat enterochromaffinlike (ECL) cells was presented recently. We have investigated the gastrin-evoked secretory activation and adaptation of ECL cells in intact rats over a time span of a few minutes to several hours. METHODS: Fasted rats received a maximally effective dose of synthetic human Leu15-gastrin-17 by continuous intravenous infusion. ECL cell ultrastructure and ECL cell-related parameters (e.g., mucosal histamine and pancreastatin concentrations, histidine decarboxylase [HDC] activity, and messenger RNA [mRNA] concentration) were analyzed. RESULTS: Gastrin reduced the number of cytoplasmic vesicles in ECL cells while reducing the concentrations of histamine and pancreastatin in the oxyntic mucosa. The effects were maximal within a few hours after the start of gastrin infusion. The concentration of pancreastatin in serum was elevated for the duration of the study. The mucosal concentrations of histamine and pancreastatin returned to prestimulation values after 4-6 hours. The HDC activity and mRNA concentration increased progressively until after 6-8 hours of gastrin infusion. CONCLUSIONS: Gastrin promptly degranulates the ECL cells, releasing histamine and pancreastatin from the vesicles. Synthesis of histamine and pancreastatin is accelerated, a process associated with renewal of vesicles. The increase in HDC activity and mRNA concentration continues for several hours after restoration of the vesicles.
BACKGROUND/AIMS: Evidence for gastrin-induced histamine secretion from isolated rat enterochromaffinlike (ECL) cells was presented recently. We have investigated the gastrin-evoked secretory activation and adaptation of ECL cells in intact rats over a time span of a few minutes to several hours. METHODS: Fasted rats received a maximally effective dose of synthetic human Leu15-gastrin-17 by continuous intravenous infusion. ECL cell ultrastructure and ECL cell-related parameters (e.g., mucosal histamine and pancreastatin concentrations, histidine decarboxylase [HDC] activity, and messenger RNA [mRNA] concentration) were analyzed. RESULTS:Gastrin reduced the number of cytoplasmic vesicles in ECL cells while reducing the concentrations of histamine and pancreastatin in the oxyntic mucosa. The effects were maximal within a few hours after the start of gastrin infusion. The concentration of pancreastatin in serum was elevated for the duration of the study. The mucosal concentrations of histamine and pancreastatin returned to prestimulation values after 4-6 hours. The HDC activity and mRNA concentration increased progressively until after 6-8 hours of gastrin infusion. CONCLUSIONS:Gastrin promptly degranulates the ECL cells, releasing histamine and pancreastatin from the vesicles. Synthesis of histamine and pancreastatin is accelerated, a process associated with renewal of vesicles. The increase in HDC activity and mRNA concentration continues for several hours after restoration of the vesicles.