scholarly journals Central site of inhibitory action of bombesin on gastric acid secretion in rats.

1987 ◽  
Vol 45 (2) ◽  
pp. 129-133 ◽  
Author(s):  
Yasunobu OKUMA ◽  
Kunihiko YOKOTANI ◽  
Yoshitsugu OSUMI
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action

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

scholarly journals Central Site of Inhibitory Action of Bombesin on Gastric Acid Secretion in Rats

1987 ◽  
Vol 45 (2) ◽  
pp. 129-133
Author(s):  
Yasunobu OKUMA ◽  
Kunihiko YOKOTANI ◽  
Yoshitsugu OSUMI
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action

scholarly journals Inhibition of Gastric Acid Secretion by Unfractionated and Low Molecular Weight Heparins in the Rat

2006 ◽  
Vol 6 ◽  
pp. 221-230
Author(s):  
Omar M.E. Abdel Salam ◽  
Ayman R. Baiuomy ◽  
Amany Ameen
Keyword(s):  
Molecular Weight ◽  
Risk Factor ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Intraperitoneal Administration ◽  
Low Molecular Weight ◽  
Gastric Erosions ◽  
Low Molecular Weight Heparins

The majority of patients receiving heparin preparations are at stress, which is a risk factor for the development of gastric erosions. Our aim was to examine the effect of unfractionated heparin (UFH) and low molecular weight heparins (LMWHs) on gastric acid secretion. Gastric acid secretion was induced in urethane-anesthetized rats by distention of the stomach (2 ml saline for 2 h) in addition to histamine or bethanechol stimulation. Distension-stimulated acid secretion (2 ml for 2 h) was significantly inhibited by intraperitoneal administration of UFH (2000 IU/kg, 19% reduction), enoxaparin (180 or 360 IU/kg, 59.2 and 87.1%, reduction, respectively), nadroparin (1000 or 2000 IU/kg, 36 and 60.7% reduction, respectively), and tinzaparin (3000 IU/kg, 41.3% reduction). All tested heparins also suppressed acid secretion in response to distention and histamine or bethanechol stimulation. Pretreatment with indomethacin did not abolish the gastric inhibitory action of nadroparin. After truncal vagotomy or atropine, nadroparin failed to inhibit acid secretion stimulated by histamine. Ganglionic blockade with guanethidine abolished the gastric inhibitory action of nadroparin or UFH. It is concluded that both UFH and LMWHs administered peripherally inhibit stimulated gastric acid secretion in the rat. This effect of heparins is determined by cholinergic and partly by adrenergic mechanisms.

scholarly journals Inhibitory action of E3810, a new H+-K+ ATPase inhibitor, on H+-K+ ATPase anil gastric acid secretion in vitro

1989 ◽  
Vol 49 ◽  
pp. 196
Author(s):  
Hideaki Fujisaki ◽  
Kiyoshi Oketani ◽  
Hisashi Shibata ◽  
Manabu Murakami ◽  
Tsuneo Wakabayashi ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Atpase Inhibitor

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)

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.

An hypothesis for discovery of inhibitors of gastric acid secretion

1964 ◽  
Vol 207 (3) ◽  
pp. 613-618 ◽  
Author(s):  
Marian E. LeFevre ◽  
Edmund J. Gohmann ◽  
Warren S. Rehm
Keyword(s):  
Carbonic Anhydrase ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Electrical Resistance ◽  
Inhibitory Action ◽  
Potential Difference ◽  
Ammonium Ions ◽  
Working Hypothesis

Davenport discovered that thiocyanate inhibits gastric acid secretion. The original working hypothesis, that this action of thiocyanate is due to inhibition of carbonic anhydrase, was successful in stimulating further work but is now no longer tenable. We propose a new working hypothesis according to which the inhibitory action is dependent on the presence of a nitrogen with a pair of unshared electrons. This hypothesis was tested by studying the effects of nitrite, cyanate, and ammonium ions on the in vitro frog's stomach. It was found that the addition of these compounds to the nutrient side reversibly inhibits H+ secretion in the same concentration range as that found for thiocyanate, i.e., 0.5–10 mm. Reduction of the H+ rate to approximately zero was associated with an increase in the transmucosal potential difference and electrical resistance to levels characteristic of the resting stomach. Acetate and nitrate in the same and higher concentrations did not inhibit the H+ rate. The hypothesis has been fruitful in that three new gastric inhibitors have been discovered, and it is hoped that it will be successful in stimulating much further work before it too becomes untenable.

scholarly journals Inhibitory action of E3810 on H+, K+-ATPase and gastric acid secretion in vitro.

1993 ◽  
Vol 102 (6) ◽  
pp. 389-397 ◽  
Author(s):  
Hideaki FUJISAKI ◽  
Kiyoshi OKETANI ◽  
Hisashi SHIBATA ◽  
Manabu MURAKAMI ◽  
Masatoshi FUJIMOTO ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action

Inhibitory action of peptide YY on gastric acid secretion

1987 ◽  
Vol 253 (3) ◽  
pp. G298-G302 ◽  
Author(s):  
Y. S. Guo ◽  
M. Fujimura ◽  
F. Lluis ◽  
Y. Tsong ◽  
G. H. Greeley ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Inhibitory Action ◽  
Peptide Yy ◽  
Dependent Manner ◽  
Inhibitory Mechanism ◽  
Cholinergic Pathways ◽  
The Face ◽  
Dose Dependent

The purpose of this study is to investigate the effect of peptide YY (PYY) on pentagastrin-, histamine-, and bethanechol-stimulated gastric acid secretion and the possible mechanisms by which PYY inhibits gastric acid secretion. Six mongrel dogs with chronic gastric and duodenal fistulas were given an intravenous infusion of pentagastrin (0.5 microgram . kg-1 . h-1), histamine (18 micrograms . kg-1 . h-1), or bethanechol (80 micrograms . kg-1 . h-1) either alone or simultaneously with intravenous PYY (100, 200, 400, pmol . kg-1 . h-1). PYY (100, 200, 400 pmol . kg-1 . h-1) inhibited pentagastrin-stimulated gastric acid secretion in a dose-dependent manner. PYY (400 pmol . kg-1 . h-1) did not depress bethanechol-stimulated gastric acid secretion. PYY (400 pmol . kg-1 . h-1) also failed to inhibit histamine-stimulated gastric acid secretion. Furthermore, PYY inhibit pentagastrin-stimulated gastric acid secretion in the face of atropine, vagotomy, or indomethacin treatment. These findings indicate that the inhibitory action of PYY on gastric acid secretion is in part independent of long and short cholinergic pathways. These findings also indicate that the inhibitory mechanism of PYY is independent of prostaglandin synthesis. Our findings are discussed in relation to previous reports regarding the effects of PYY on gastric acid secretion.

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