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.

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.

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 The mechanism of inhibitory action of secretin on gastric acid secretion in conscious rats.

1995 ◽  
Vol 488 (2) ◽  
pp. 501-508 ◽  
Author(s):  
K Shimizu ◽  
P Li ◽  
K Y Lee ◽  
T M Chang ◽  
W Y Chey
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Conscious Rats

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.

Pilocarpine-induced Salivation and Thirst in Conscious Rats

2006 ◽  
Vol 85 (1) ◽  
pp. 64-68 ◽  
Author(s):  
N. Sato ◽  
K. Ono ◽  
E. Honda ◽  
K. Haga ◽  
M. Yokota ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Receptor Antagonist ◽  
Muscarinic Receptor ◽  
Water Intake ◽  
Receptor Agonist ◽  
Salivary Secretion ◽  
Parotid Glands ◽  
Conscious Rats ◽  
The Central Nervous System

The muscarinic receptor agonist pilocarpine is widely used as a sialogogue. It has been well-established that it also induces water intake in animals. However, the mechanisms underlying the relationships between these events are unknown. To address this problem, we examined water intake and parotid salivary secretion in conscious rats. Intraperitoneally injected pilocarpine increased both water intake and salivary secretion. Intracerebroventricularly injected pilocarpine also induced water intake, but not salivary secretion. Intracerebroventricularly applied atropine, a muscarinic receptor antagonist, suppressed the water intake produced by pilocarpine applied intraperitoneally and intracerebroventricularly. However, it did not affect the salivary secretion induced by pilocarpine applied peripherally. We conclude that peripherally applied pilocarpine affects the parotid glands and the thirst center in the central nervous system, while it may induce salivary secretion mainly via peripheral responses, but water intake mainly via the central nervous system.

CRF initiates biological actions within the brain that are observed in response to stress

1987 ◽  
Vol 252 (1) ◽  
pp. R34-R39 ◽  
Author(s):  
H. J. Lenz ◽  
A. Raedler ◽  
H. Greten ◽  
M. R. Brown
Keyword(s):  
Heart Rate ◽  
Nervous System ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Plasma Catecholamine ◽  
Biological Actions

Corticotropin-releasing factor (CRF) is thought to be an endogenous mediator of adrenocorticotropic hormone release following stress. We examined if CRF initiates further biological actions that are observed in response to stressful events. Male beagle dogs (10–12 kg) were fitted with a chronic intracerebroventricular cannula, intra-arterial and intravenous catheters, as well as a gastric fistula. Synthetic human CRF was microinjected into the third cerebral ventricle in conscious animals. CRF (0.1–1.0 nmol/kg) significantly (P less than 0.01) increased plasma concentrations of epinephrine, norepinephrine, glucagon, and glucose and elevated mean arterial pressure and heart rate. Pretreatment of the animals with the ganglionic blocking agent chlorisondamine completely abolished the increases in plasma catecholamine and glucose concentrations as well as the elevations in blood pressure and heart rate. CRF significantly (P less than 0.01) inhibited gastric acid secretion, but not plasma gastrin concentrations stimulated by an 8% liquid peptone meal. The gastric inhibitory action of CRF was completely prevented by chlorisondamine and, in part, by naloxone and a vasopressin antagonist. In contrast, bilateral truncal vagotomy did not affect the gastric inhibitory action of CRF. The results of this study indicate that CRF acts within the central nervous system to increase plasma glucose and glucagon concentrations, mean arterial pressure, and heart rate by activation of the autonomic nervous system. CRF inhibits meal-stimulated gastric acid secretion by activation of the sympathetic nervous system and, in part, by opiate and vasopressin-dependent pathways and not by inhibition of gastrin release.(ABSTRACT TRUNCATED AT 250 WORDS)

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