Centrally administered NPY stimulated gastric acid and pepsin secretion by a vagally mediated mechanism

Matsuda, Masayuki; Aono, Mitsuru; Moriga, Motoyuki; Okuma, Minoru

doi:10.1016/0167-0115(91)90251-b

Cited by 28 publications

(21 citation statements)

References 25 publications

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“…In line with the latter findings, injection of NPY (0.2-0.8 pg) into the 3rd ventricle was previously reported to have no effect on basal gastric acid secretion in rats (Humphreys et al, 1988). At higher doses (2.5 and 35 pg), however, intracisternal or intracerebroventricular injection of NPY increased basal or pentagastrin-stimulated gastric acid secretion in urethane-anaesthetized rats (Matsuda et al, 1991;Geoghegan et al, 1992). The interaction between NPY and CRF is peptide specific since intracisternal injection of NPY at a dose preventing CRF antisecretory action did not alter bombesin-or hIL-ip-induced inhibition of pentagastrin- P < 0.05 compared with respective saline-microinjected group stimulated acid secretion.…”

Section: Discussionsupporting

confidence: 71%

Central neuropeptide Y and the sigma ligand, JO 1784, reverse corticotropin‐releasing factor‐induced inhibition of gastric acid secretion in rats

Gué¹,

Yoneda

Mönnikes

et al. 1992

British J Pharmacology

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4 CRF (3 jig) microinjected into the hypothalamic paraventricular nucleus (PVN) and the lateral hypothalamus (LH) inhibited pentagastrin-stimulated gastric acid secretion by 61% and 51%; NPY (0.03 gg) or JO 1784 (0.03 gig) microinjected into the PVN had no effect by themselves but blocked CRF antisecretory action. Microinjection into the LH had no effect. 5 In conclusion, NPY and JO 1784 (a sigma ligand) interacts with CRF in the PVN to block CRF-induced inhibition of pentagastrin-stimulated gastric acid secretion. The central action of JO 1784 and NPY is specific to CRF and may involve sigma binding sites.

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Section: Discussionsupporting

confidence: 71%

Central neuropeptide Y and the sigma ligand, JO 1784, reverse corticotropin‐releasing factor‐induced inhibition of gastric acid secretion in rats

Gué¹,

Yoneda

Mönnikes

et al. 1992

British J Pharmacology

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“…Nitric oxide is hypothesized to serve as an intermediary in the gastric acid suppression induced by endotoxin, cytokines, or stress (13,14,27). Interestingly, while several orexigenic hormones have been implicated in vagal stimulation of gastric acid production, nesfatin is the only anorexigenic hormone confirmed to inhibit vagally mediated gastric acid production (11,28,46). Vagovagal circuits relayed through the DVC regulate a variety of gastric functions, including the secretion of gastric acid (8,9).…”

Section: Discussionmentioning

confidence: 99%

Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats

Xia

Fritze

et al. 2012

American Journal of Physiology-Gastrointestinal and Liver Physi

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MW. Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats. Am J Physiol Gastrointest Liver Physiol 303: G570 -G577, 2012. First published June 21, 2012; doi:10.1152/ajpgi.00178.2012.-Nesfatin-1, a novel hypothalamic peptide, inhibits nocturnal feeding behavior and gastrointestinal motility in rodents. The effects of nesfatin-1 on gastrointestinal secretory function, including gastric acid production, have not been evaluated. Nesfatin-1 was injected into the fourth intracerebral ventricle (4V) of chronically cannulated rats to identify a nesfatin dose sufficient to inhibit food intake. Nesfatin-1 (2 g) inhibited dark-phase food intake, in a dose-dependent fashion, for Ͼ3 h. Gastric acid production was evaluated in urethane-anesthetized rats. Nesfatin-1 (2 g) was introduced via the 4V following endocrine stimulation of gastric acid secretion by pentagastrin (2 g·kg Ϫ1 ·h Ϫ1 iv), vagal stimulation with 2-deoxy-D-glucose (200 mg/kg sc), or no stimulus. Gastric secretions were collected via gastric cannula and neutralized by titration to determine acid content. Nesfatin-1 did not affect basal and pentagastrin-stimulated gastric acid secretion, whereas 2-deoxy-D-glucosestimulated gastric acid production was inhibited by nesfatin-1 in a dose-dependent manner. c-Fos immunofluorescence in brain sections was used to evaluate in vivo neuronal activation by nesfatin-1 administered via the 4V. Nesfatin-1 caused activation of efferent vagal neurons, as evidenced by a 16-fold increase in the mean number of c-Fos-positive neurons in the dorsal motor nucleus of the vagus (DMNV) in nesfatin-1-treated animals vs. controls (P Ͻ 0.01). Finally, nesfatin-induced Ca 2ϩ signaling was evaluated in primary cultured DMNV neurons from neonatal rats. Nesfatin-1 caused dosedependent Ca 2ϩ increments in 95% of cultured DMNV neurons. These studies demonstrate that central administration of nesfatin-1, at doses sufficient to inhibit food intake, results in inhibition of vagally stimulated secretion of gastric acid. Nesfatin-1 activates DMNV efferent vagal neurons in vivo and triggers Ca 2ϩ signaling in cultured DMNV neurons. gastric hormones; intracellular calcium; dorsal motor nucleus of the vagus NESFATIN-1, an 82-amino acid peptide derived from the parent peptide nucleobindin-2, was first identified as a satiety molecule in the hypothalamus by Oh et al. (33). Inhibition of rodent nocturnal feeding behavior by nesfatin-1 administered into the intracranial ventricles has been consistently observed (18,25,34,40,42). Most centrally acting peptides that influence food intake also regulate the processes of digestion, including gastrointestinal motility and secretory function (45). In rodents, nesfatin-1 inhibits gastroduodenal motility and gastric empty-

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“…Systemic administration of NPY stimulates duodenal alkaline secretion, through vagal non-cholinergic neuronal mechanisms (Pascaud et al, 1993). The release of immunoreactive-NPY from the rat isolated stomach can be provoked by acetylcholine, probably through nicotinic-receptor stimulation of intrinsic ganglia (McIntosh et al, 1992), while intracerebroventricular administration of NPY stimulated both gastric acid and pepsin secretion through a vagally mediated process (Matsuda et al, 1991). By contrast, injection of NPY into the rat hypothalamic paraventricular nucleus inhibited acid secretion through a mechanism involving the suppression of vagal cholinergic tone following activation of M2-adrenoceptors, but did not affect gastric mucosal blood flow (Humphreys et al, 1992).…”

Section: Microvascular Ischaemia and Injurymentioning

confidence: 99%

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1993

British J Pharmacology

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Centrally administered NPY stimulated gastric acid and pepsin secretion by a vagally mediated mechanism

Cited by 28 publications

References 25 publications

Central neuropeptide Y and the sigma ligand, JO 1784, reverse corticotropin‐releasing factor‐induced inhibition of gastric acid secretion in rats

Central neuropeptide Y and the sigma ligand, JO 1784, reverse corticotropin‐releasing factor‐induced inhibition of gastric acid secretion in rats

Nesfatin-1 inhibits gastric acid secretion via a central vagal mechanism in rats

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