Mechanism Of Gastrin Release Research Articles

Regulatory mechanism of bombesin on gastrin release

Bombesin has been demonstrated to stimulate gastrin release by an atropine‐resistant mechanism. In the present study, the effects of truncal vagotomy and chemical sympathectomy on the gastrin release by exogenous and endogenous bombesin using rat antral mucosa in tissue culture were studied. Exogenous bombesin 10‐8 mol/l significantly stimulated gastrin release. The stimulation of gastrin release by bombesin was abolished by truncal vagotomy, but not altered by chemical sympathectomy. Bombesin antiserum inhibited gastrin release by blocking the effect of endogenous bombesin. The inhibition of gastrin release by bombesin antiserum was abolished by truncal vagotomy, but not altered by chemical sympathectomy. In addition, the concentrations of bombesin‐like immunoreactivity in antral mucosa were not altered by truncal vagotomy. These results suggest that the mechanism of gastrin release by bombesin is influenced by non‐cholinergic local nerves under vagal control.

Gastrin release and gastric secretion induced by dimethylxanthine in man.

Gastrin release and gastric secretion in response to i.v. dimethylxanthine (2 mg/kg for 5 min followed by a 55-min infusion of 2.5 mg/kg) were studied in 25 normal subjects. Gastrin release was significantly stimulated, whereas gastric acid and pepsin secretion was inhibited. The adenylcyclase activation may, therefore, play a role in the mechanism of gastrin release. Moreover, dimethylxanthine seems to be a useful aid in studies on G-cell function in man.

Ultrastructures of G cells and the mechanism of gastrin release before and after selective vagotomy with pyloroplasty.

A combined, electron microscope and radioimmunoassay investigation was carried out on the G cells and blood gastrin levels in patients who received either selective vagotomy (SV) plus pyloroplasty (P) or selective vagotomy plus antrectomy (A) for duodenal ulcer.1. After SV+P, G cells did not show any degenerative or hypofunctional signs in their fine structure, but their secretory granules trended towards the cell base, suggesting a presecretory state. Six months postoperatively, the G cells were markedly increased in number (hyperplasia). In accordance, basal gastrin levels were elevated (hypergastrinemia). After SV+A, which caused better prognosis, blood gastrin levels dropped more or less conspiciously as the main source of G cells had been removed.2. G cells denervated by surgery (SV+P), reacted to the stimuli of meat extract by releasing their granules and elevating blood gastrin levels, as the innervated G cells do. The response of G cells to the luminal stimuli is thus not believed to be essentially related to nerves.3. The denervated G cells also could, as innervated ones, release gastrin in response to insulin hypoglycemia. Thus it is proposed that this stimulation is not mediated by the vagal nerve.4. Gastrin release from the G cell was evidenced in this study as emiocytotic granule release from the cell base. The frequency of the Ω-shaped granule openings found in the electron microscope well corresponded to the gastrin levels in the blood.

247) - Mechanism of gastrin release from denervated antral pouches

247) - Mechanism of gastrin release from denervated antral pouches

A duodenal role in gastrin release.

Observations on the plasma gastrin response to feeding protein in patients with the dumping syndrome, patients with pyloric stenosis, and patients asymptomatic after gastric surgery suggested that the duodenum might be important in the mechanism of gastrin release. This duodenal role was confirmed by the finding that when the stimulus was placed directly in the duodenum peak gastrin levels occurred earlier than when the stimulus was placed directly in the stomach.

Studies on the site and mechanism of gastrin release.

Previous studies from this laboratory, as well as elsewhere, have indicated that the antrum of the stomach is the chief or sole source of the gastric-secretion-stimulating hormone, gastrin. Complete excision of the gastric antrum in dogs practically abolishes the secretion of gastric juice from a vagusdenervated Heidenhain pouch.1Exclusion of the antrum from the alimentary tract produces a similar reduction in secretion from the Heidenhain pouch, and this is restored if the antrum is replaced in its normal position or transplanted to the duodenum as a diverticulus. Transplantation of the antrum to the colon produces a marked hypersecretion of gastric juice from the Heidenhain pouch. On the other hand, transplantation of similar pouches fashioned from the corpus or fundus of the stomach into the duodenum or colon produces no stimulation of secretion.2If the antrum is converted into a vagus-denervated isolated pouch in an animal also provided with