Cholecystokinin inhibits gastric acid secretion through type "A" cholecystokinin receptors and somatostatin in rats

1992 ◽  
Vol 263 (3) ◽  
pp. G287-G292 ◽  
Author(s):  
K. C. Lloyd ◽  
H. E. Raybould ◽  
J. H. Walsh
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Type A ◽  
Inhibitory Effect ◽  
Cck Receptors ◽  
Cholecystokinin Receptors ◽  
Maximum Inhibition ◽  
Vagal Reflex ◽  
Dependent Pathway

The purpose of this study was to determine whether selective antagonism of type "A" cholecystokinin (CCK) receptors blocks inhibition of gastric acid secretion produced by CCK and whether this inhibition is mediated through either a somatostatin-dependent pathway or a vago-vagal reflex. Intravenous infusion of CCK (0.04-10 nmol.kg-1.h-1) dose dependently inhibited pentagastrin-stimulated gastric acid secretion in urethan-anesthetized rats, with a 50% inhibitory dose of 0.9 nmol.kg-1.h-1 and a maximum inhibition of approximately 50%. Blockade of type A CCK receptors using the selective type A receptor antagonist MK-329 completely reversed the inhibitory effect produced by a maximal dose (4 nmol.kg-1.h-1) of CCK. Immunoneutralization of endogenous somatostatin by administration of somatostatin monoclonal antibody abolished the inhibition produced by CCK. Concentrations of somatostatin in portal venous plasma were significantly increased after CCK administration; the increase in somatostatin was blocked by pretreatment with MK-329. In contrast, CCK-induced inhibition of gastric acid secretion was unaltered after perivagal capsaicin treatment. These results indicate that CCK inhibits gastric acid secretion in rats by activation of type A CCK receptors and through release of endogenous somatostatin.

Stimulation of neurons in rat ARC inhibits gastric acid secretion via hypothalamic CRF1/2- and NPY-Y1 receptors

2003 ◽  
Vol 285 (6) ◽  
pp. G1075-G1083 ◽  
Author(s):  
Johannes J. Tebbe ◽  
Silke Mronga ◽  
Martin K.-H. Schäfer ◽  
Jens Rüter ◽  
Peter Kobelt ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Excitatory Amino Acid ◽  
Inhibitory Effect ◽  
Receptor Subtypes ◽  
Npy Receptor ◽  
Y1 Receptors ◽  
Open Question

Neuropeptide Y (NPY) neuronal projections from the arcuate nucleus (ARC) have been proposed to target corticotropin-releasing factor (CRF)-positive neurons in the paraventricular nucleus (PVN) as part of the ARC-PVN axis. The existence of a positive feedback loop involving CRF receptors in the PVN has been suggested. Exogenous NPY and CRF in the PVN have been shown to inhibit gastric acid secretion. Recently, we have demonstrated that activation of ARC neurons inhibits gastric acid secretion via vagal pathways. To what extent NPY- and CRF-mediated mechanisms in the PVN contribute to the CNS modulation of gastric acid secretion is still an open question. In the present study, we performed consecutive bilateral microinjections of antagonists to NPY receptor subtypes Y1 and Y2 and to CRF1/2 receptors in the PVN and of the excitatory amino acid kainate in the ARC to assess the role of NPY- and CRF-mediated mechanisms in the kainate-induced effects on gastric acid secretion. Gastric acid secretion was measured at the basal condition and during pentagastrin (16 μg/kg body wt) stimulation. Microinjection of vehicle in the PVN and kainate in the ARC decreased gastric acid secretion. Microinjection of the specific NPY-Y1 receptor antagonist BIBP-3226 (200 pmol) and the nonspecific CRF1/2 antagonist astressin (30 pmol) in the PVN abolished the inhibitory effect of neuronal activation in the ARC by kainate on gastric acid secretion. The CRF antagonist astressin was more effective. Pretreatment with the NPY-Y2 receptor antagonist BIIE-0246 (120 pmol) in the PVN had no significant effect. Our results indicate that activation of neurons in the ARC inhibits gastric acid secretion via CRF1/2 and NPY-Y1 receptor-mediated pathways in the PVN.

Inhibitory effect of neurotensin on gastric acid secretion in rats

1990 ◽  
Vol 35 (4) ◽  
pp. 439-443 ◽  
Author(s):  
Robert A. Hammer ◽  
Richard E. Hernandez ◽  
Ann Shepard
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Effect

Recent advances in the physiology of gastrin

1968 ◽  
Vol 170 (1018) ◽  
pp. 81-88 ◽  
Keyword(s):  
Gastric Secretion ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Chemical Mechanism ◽  
Antral Mucosa ◽  
Aqueous Extracts ◽  
Gastric Digestion ◽  
Hormonal Mechanism ◽  
Vagal Reflex

On 18 May 1905 there was presented at a meeting of this Society a paper in the name of John Sydney Edkins entitled ‘On the chemical mechanism of gastric secretion’ (Edkins 1905). It described experiments in which simple aqueous extracts of antral and fundic mucosa were tested for their power to stimulate gastric secretion when injected as single intravenous doses into anaesthetized cats. Antral extracts excited a secretion of acid and pepsin; fundic extracts did not. Edkins concluded that certain cells in the antral mucosa contained a principle which he named ‘gastrin’; this, he considered, entered the circulation during gastric digestion and stimulated the fundic glands to further activity following on the initial vagal reflex excited by the eating of the meal. These experiments, later recounted in detail (Edkins 1906) initiated more than 40 years of controversy as to the existence of a gastric antral hormone. When attempts were made to confirm and extend Edkins’s observations it was soon discovered that a stimulant of gastric acid secretion could be found not only in antral mucosa but also in many other tissues; and when eventually this ubiquitous agent was identified as histamine (Barger & Dale 1910; Dale & Laidlaw 1910; Popielski 1919) it was widely concluded that the activity of Edkins’s antral extract was due to the presence in it of this substance. The situation was further confused by the failure of apparently well-designed attempts to prove by physio­logical experiment that an antral hormonal mechanism existed, whatever the nature of the hormone. For example, Ivy & Whitlow (1922) and Priestley & Mann (1932) provided dogs with fundic and antral pouches and irrigated the latter with solutions regarded at the time as likely to cause a release of the hormone; but no response from the fundic pouch could be detected, and many years elapsed before the probable reason for such failure became appreciated.

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