Comparative Evaluation of the Role of Endogenous Gastrin in Basal Acid Secretion in Conscious Rats Provided with Chronic Fistula and Pylorus Ligation

Nishida, Akito; Uchida-Kobayashi, Ayumi; Takemoto, Yukihiro; Akuzawa, Shinobu; Miyata, Keiji

doi:10.1254/jjp.71.223

Cited by 9 publications

(4 citation statements)

References 24 publications

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“…We suggest the following explanation: Basal acid secretion, as measured by pylorus ligation, may not reflect resting, non‐stimulated/basal secretory activity, as pylorus ligation itself stimulates acid secretion in a neurogenic manner of vagal origin, and acid response depends on vagal activity 25,47–50 . Furthermore, pylorus ligation also affects carbachol‐stimulated acid secretion, potentially confounding results, as FSL rats did not respond to carbachol in comparison with FRL rats.…”

Section: Discussionmentioning

confidence: 96%

Altered physiology of acid secretion in depression‐prone Flinders rats results in exacerbated NSAID and stress‐induced gastric damage

Padol

Wang

Hunt

2011

Neurogastroenterology Motil

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Section: Discussionmentioning

confidence: 96%

Altered physiology of acid secretion in depression‐prone Flinders rats results in exacerbated NSAID and stress‐induced gastric damage

Padol

Wang

Hunt

2011

Neurogastroenterology Motil

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“…It is traditionally argued that vagal excitation stimulates the parietal cell through cholinergic mechanisms since acid secretion can be inhibited by atropine (and pirenzepine) (Ekelund et al 1987; Riedel et al 1988). Paradoxically, however, cholinergic agents, such as carbachol and bethanechol, are poor secretagogues in the chronic gastric fistula rat (Ding & Håkanson, 1996; Nishida et al 1996). Although the ECL cells do not seem to operate under cholinergic control (Lindström et al 1997; Lindström & Håkanson, 2001; Norlén et al 2001), they do respond with secretory activation to a number of neuropeptides present in neurones in the stomach wall, e.g.…”

Section: Discussionmentioning

confidence: 99%

Section: Histamine Mobilization In Response To Vagus Stimulationmentioning

confidence: 99%

The vagus regulates histamine mobilization from rat stomach ECL cells by controlling their sensitivity to gastrin

Norlén

Ericsson

Kitano

et al. 2005

The Journal of Physiology

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The ECL cells in the oxyntic mucosa secrete histamine in response to gastrin, stimulating parietal cells to produce acid. Do they also operate under nervous control? The present study examines histamine mobilization from rat stomach ECL cells in situ in response to acute vagal excitation and to food or gastrin following vagal or sympathetic denervation. Applying the technique of microdialysis, we monitored the release of histamine by radioimmunoassay. Microdialysis probes were placed in the submucosa on either side of the stomach, 3 days before experiments. The rats were awake during microdialysis except when subjected to electrical vagal stimulation. One-sided electrical vagal stimulation raised serum gastrin and mobilized gastric histamine. However, gastrin receptor blockade prevented the histamine mobilization, indicating that circulating gastrin accounts for the response. Vagal excitation by hypoglycaemia (insulin) or pylorus ligation did not mobilize either gastrin or histamine. The histamine response to food was almost abolished by gastrin receptor blockade, and it was halved on the denervated side after unilateral subdiaphragmatic vagotomy. While the histamine response to a near-maximally effective dose of gastrin was unaffected by vagotomy, the response to low gastrin doses was reduced significantly. Abdominal ganglionic sympathectomy failed to affect the histamine response to either food or gastrin. In conclusion, gastrin is responsible for most of the food-evoked mobilization of ECL-cell histamine. The histamine response to electrical vagal stimulation reflects the effect of circulating gastrin rather than a direct action of the vagus on the ECL cells. Vagal denervation was accompanied by an impaired histamine response to food intake, probably reflecting the right-ward shift of the serum gastrin concentration-histamine response curve. The results suggest that the vagus controls the sensitivity of the ECL cells to gastrin.

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“…After confirming that pretreatment of famotidine (0.33 mg/kg BW) completely inhibited histamine-stimulated (1 mg/kg BW) acid secretion, famotidine at the pretreatment dose was administered 30 min before administration of motilin (10 μg/kg BW) and co-administration of motilin (10 μg/kg BW) and ghrelin (10 μg/kg BW). To examine the involvement of gastrin (CCK-B) receptors in motilin-stimulated gastric acid secretion, we also administered YM 022 (0.2 mg/kg BW) [ 36 , 37 ]. Vehicle or YM 022 (0.2 mg/kg BW) was administered 30 min before each drug injection.…”

Section: Methodsmentioning

confidence: 99%

Motilin Stimulates Gastric Acid Secretion in Coordination with Ghrelin in Suncus murinus

et al. 2015

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Motilin and ghrelin constitute a peptide family, and these hormones are important for the regulation of gastrointestinal motility. In this study, we examined the effect of motilin and ghrelin on gastric acid secretion in anesthetized suncus (house musk shrew, Suncus murinus), a ghrelin- and motilin-producing mammal. We first established a gastric lumen-perfusion system in the suncus and confirmed that intravenous (i.v.) administration of histamine (1 mg/kg body weight) stimulated acid secretion. Motilin (0.1, 1.0, and 10 μg/kg BW) stimulated the acid output in a dose-dependent manner in suncus, whereas ghrelin (0.1, 1.0, and 10 μg/kg BW) alone did not induce acid output. Furthermore, in comparison with the vehicle administration, the co-administration of low-dose (1 μg/kg BW) motilin and ghrelin significantly stimulated gastric acid secretion, whereas either motilin (1 μg/kg BW) or ghrelin (1 μg/kg BW) alone did not significantly induce gastric acid secretion. This indicates an additive role of ghrelin in motilin-induced gastric acid secretion. We then investigated the pathways of motilin/motilin and ghrelin-stimulated acid secretion using receptor antagonists. Treatment with YM 022 (a CCK-B receptor antagonist) and atropine (a muscarinic acetylcholine receptor antagonist) had no effect on motilin or motilin-ghrelin co-administration-induced acid output. In contrast, famotidine (a histamine H2 receptor antagonist) completely inhibited motilin-stimulated acid secretion and co-administration of motilin and ghrelin induced gastric acid output. This is the first report demonstrating that motilin stimulates gastric secretion in mammals. Our results also suggest that motilin and co-administration of motilin and ghrelin stimulate gastric acid secretion via the histamine-mediated pathway in suncus.

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Comparative Evaluation of the Role of Endogenous Gastrin in Basal Acid Secretion in Conscious Rats Provided with Chronic Fistula and Pylorus Ligation

Cited by 9 publications

References 24 publications

Altered physiology of acid secretion in depression‐prone Flinders rats results in exacerbated NSAID and stress‐induced gastric damage

Altered physiology of acid secretion in depression‐prone Flinders rats results in exacerbated NSAID and stress‐induced gastric damage

The vagus regulates histamine mobilization from rat stomach ECL cells by controlling their sensitivity to gastrin

Motilin Stimulates Gastric Acid Secretion in Coordination with Ghrelin in Suncus murinus

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