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
1989 ◽  
Vol 256 (1) ◽  
pp. G214-G219 ◽  
Author(s):  
G. Druge ◽  
A. Raedler ◽  
H. Greten ◽  
H. J. Lenz

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.


1990 ◽  
Vol 524 (2) ◽  
pp. 208-212 ◽  
Author(s):  
Myung Suk Kim ◽  
Yang Hyeok Jo ◽  
Shin Hee Yoon ◽  
Sang June Hahn ◽  
Duck Joo Rhie ◽  
...  

1987 ◽  
Vol 45 (2) ◽  
pp. 129-133
Author(s):  
Yasunobu OKUMA ◽  
Kunihiko YOKOTANI ◽  
Yoshitsugu OSUMI

2006 ◽  
Vol 6 ◽  
pp. 221-230
Author(s):  
Omar M.E. Abdel Salam ◽  
Ayman R. Baiuomy ◽  
Amany Ameen

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.


1987 ◽  
Vol 45 (2) ◽  
pp. 129-133 ◽  
Author(s):  
Yasunobu OKUMA ◽  
Kunihiko YOKOTANI ◽  
Yoshitsugu OSUMI

2002 ◽  
Vol 75 (2) ◽  
pp. 92-97 ◽  
Author(s):  
V. Sibilia ◽  
F. Pagani ◽  
F. Guidobono ◽  
V. Locatelli ◽  
A. Torsello ◽  
...  

1984 ◽  
Vol 104 (10) ◽  
pp. 1090-1094 ◽  
Author(s):  
MASAKI HAGIWARA ◽  
HIROSHI WATANABE ◽  
KEIKO KAWATA ◽  
KAZUO WATANABE

1996 ◽  
Vol 270 (1) ◽  
pp. G220-G224 ◽  
Author(s):  
S. Higashide ◽  
G. Gomez ◽  
G. H. Greeley ◽  
C. M. Townsend ◽  
J. C. Thompson

The purpose of this study was to examine whether an intermediate form of amidated gastrin, glycine-extended gastrin (Gly-G), can stimulate gastric acid secretion in conscious rats prepared with gastric fistulas. Intravenous administration of Gly-G (20 nmol.kg-1.h-1) alone for 2 h did not stimulate gastric acid secretion; however, administration of Gly-G (20 nmol.kg-1.h-1) in combination with a bolus administration of gastrin (9.5 nmol/kg) potentiated acid secretion significantly. Gastric acid secretion in response to gastrin alone and gastrin plus Gly-G (2 nmol.kg-1.h-1) was 109.1 +/- 21.6 and 170.1 +/- 27.7 mueq.kg-1.h-1, respectively (P < 0.05). Gastric acid secretion in response to gastrin alone and gastrin plus Gly-G (20 nmol.kg-1.h-1) was 84.8 +/- 17.5 and 164.1 +/- 29.3 mueq.kg-1.h-1, respectively (P < 0.05). Intravenous administration of Gly-G (20 nmol.kg-1.h-1) failed to increase histamine (1 mg/kg)-stimulated acid output. These results demonstrate that Gly-G can selectively potentiate the stimulatory effect of gastrin on acid secretion in rats and that the unprocessed form of gastrin, Gly-G, can exert a biological effect in the stomach.


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