Ghrelin Acts in the Central Nervous System to Stimulate Gastric Acid Secretion

2001 ◽  
Vol 280 (3) ◽  
pp. 904-907 ◽  
Author(s):  
Yukari Date ◽  
Masamitsu Nakazato ◽  
Noboru Murakami ◽  
Masayasu Kojima ◽  
Kenji Kangawa ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
The Central Nervous System

scholarly journals Cocaine-Amphetamine-Regulated Transcript (CART) Acts in the Central Nervous System to Inhibit Gastric Acid Secretion via Brain Corticotropin-Releasing Factor System*

Endocrinology ◽  
2000 ◽  
Vol 141 (8) ◽  
pp. 2854-2860 ◽  
Author(s):  
Toshikatsu Okumura ◽  
Hiroto Yamada ◽  
Wataru Motomura ◽  
Yutaka Kohgo
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Inhibition ◽  
Gastric Function ◽  
The Central Nervous System ◽  
The Brain

Recent study has indicated that cocaine-amphetamine-regulated transcript (CART) is an anorectic chemical in the brain. In the present study, we examined the hypothesis that CART may act in the central nervous system to alter gastric function. Food consumption, gastric acid secretion, and gastric emptying were measured after injection of CART into the cerebrospinal fluid in 24-h fasted Sprague Dawley rats. Central injection of CART inhibited food intake, gastric acid secretion, and gastric emptying. In contrast, ip injection of CART failed to inhibit gastric acid secretion and gastric emptying, suggesting that CART acts in the brain to suppress gastric acid secretion and gastric emptying. In the vagotomized animals, centrally administered CART did inhibit pentagastrin-stimulated gastric acid secretion. The CART-induced acid inhibition was also observed in rats treated with indomethacin, a cyclooxygenase inhibitor. In contrast, pretreatment with central administration of a CRF receptor antagonist,α -helical CRF9–41, completely blocked the central CART-induced inhibition of gastric acid secretion. All these results suggest that CART acts in the brain to inhibit gastric function via brain CRF system. The vagal pathway and the prostaglandin system are not involved in the acid inhibition.

Pathways mediating CRF-induced inhibition of gastric acid secretion in rats

1989 ◽  
Vol 256 (1) ◽  
pp. G214-G219 ◽  
Author(s):  
G. Druge ◽  
A. Raedler ◽  
H. Greten ◽  
H. J. Lenz
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Plasma Concentrations ◽  
Conscious Rats ◽  
The Central Nervous System

The pathways involved in mediating the central nervous system actions of corticotropin-releasing factor (CRF) on gastric acid secretion were examined in conscious rats. CRF (0.1-2.0 nmol) given cerebroventricularly inhibited gastric acid secretion stimulated by pentagastrin (P less than 0.01). This effect was abolished by cerebroventricular but not intravenous administration of a specific CRF receptor antagonist, alpha-helical CRF-(9-41). Ganglionic blockade with chlorisondamine chloride, noradrenergic blockade with bretylium, or adrenalectomy abolished the gastric inhibitory action of CRF whereas truncal vagotomy or opiate blockade with naloxone did not. A vasopressin receptor antagonist significantly inhibited but did not abolish the gastric inhibitory action of CRF. An intravenous infusion of epinephrine that mimicked the epinephrine plasma concentrations which were observed after cerebroventricular administration of CRF did not alter pentagastrin-stimulated gastric acid secretion. These results indicate that CRF acts within the central nervous system to inhibit gastric acid secretion by a specific receptor-mediated event. Inhibition of gastric acid secretion by CRF in conscious rats is mediated by efferent fibers of the sympathetic nervous system and in part by a vasopressin-dependent pathway but not by the parasympathetic nervous system, adrenal epinephrine release, or opiate-sensitive pathways.

CNS regulation of gastric and autonomic functions in dogs by gastrin-releasing peptide

1988 ◽  
Vol 255 (3) ◽  
pp. G298-G303
Author(s):  
H. J. Lenz
Keyword(s):  
Nervous System ◽  
Gastric Emptying ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Left Gastric Artery ◽  
Gastric Artery ◽  
Ganglionic Blockade ◽  
The Central Nervous System ◽  
Artery Flow

The central nervous system effects of canine gastrin-releasing peptide (GRP) were studied on gastric acid secretion, emptying, blood flow, and the autonomic nervous system in conscious dogs. GRP injected into the third cerebral ventricle significantly (P less than 0.01) increased plasma epinephrine but not norepinephrine concentrations. GRP (0.1-1.0 nmol/kg) significantly decreased gastric acid secretion stimulated by an 8% peptone meal, delayed gastric emptying of the liquid peptone meal, and increased left gastric artery flow. Ganglionic blockade, truncal vagotomy, or adrenalectomy did not abolish the inhibitory effect of GRP on gastric acid secretion. However, ganglionic blockade or vagotomy abolished the GRP-induced inhibition of gastric emptying, and ganglionic blockade or adrenalectomy abolished the GRP-induced increases in left gastric artery flow and plasma epinephrine concentrations. An intravenous infusion of epinephrine that produced similar plasma concentrations of epinephrine that were observed after cerebroventricular injection of GRP mimicked the increase in left gastric artery flow induced by GRP. It is concluded that 1) GRP acts within the central nervous system to activate the sympathoadrenal axis, 2) GRP inhibits gastric emptying of a liquid meal by a vagally dependent mechanism and enhances left gastric artery flow by the release of epinephrine from the adrenal medulla, and 3) the pathway(s) that mediate the GRP-induced inhibition of gastric acid in the dog remain unknown.

Cytoprotective effect of centrally administered neurotensin on stress-induced gastric ulcers

1982 ◽  
Vol 242 (4) ◽  
pp. G342-G346
Author(s):  
C. B. Nemeroff ◽  
D. E. Hernandez ◽  
R. C. Orlando ◽  
A. J. Prange
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Gastric Ulcers ◽  
Cytoprotective Effect ◽  
Gastrointestinal Tissue

Neurotensin, a peptide common to brain and gastrointestinal tissue, has been reported common to brain and gastrointestinal tissue, has been reported to inhibit both gastric acid secretion and gastric mucosal blood flow after central nervous system administration in rats. Therefore, the effect of intracisternal neurotensin on the development of gastric ulcers induced by cold-plus-restraint stress in the rat was studied. Following intracisternal injection, neurotensin (20-30 micrograms) significantly inhibited the development of gastric ulcers in this model. This effect was shown to be both dose related and route specific, inasmuch as neither lower doses of intracisternal neurotensin nor intravenous neurotensin were cytoprotective. In addition, potential actions of central neurotensin that may have mediated this beneficial effect were tested by administering somatostatin or oxotremorine intracisternally and cimetidine or haloperidol intraperitoneally. In contrast to intracisternal neurotensin, none of these substances reduced the incidence of gastric ulcers in this model. This was true despite the fact that cimetidine, but not neurotensin, significantly increased gastric pH. Finally, when cold-plus-restraint-stressed rats were pretreated with indomethacin, an inhibitor of prostaglandin synthesis, the cytoprotective effect of neurotensin was completely abolished. These results suggest that intracisternal neurotensin exerts a significant cytoprotective effect for stress-induced gastric ulcers in rats. This effect, which is mediated by the central nervous system, does not appear to be related to changes in body temperature, neuroleptic-like properties, or gastric acid secretion but requires an intact prostaglandin synthetic pathway.

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