Effect of Two Types of β-Adrenergic Blockade on Gastric Acid Secretion During Pentagastrin Stimulation in Non-vagotomized and in Vagotomized Gastric Fistula Dogs

1979 ◽  
Vol 14 (7) ◽  
pp. 857-864 ◽  
Author(s):  
F. Gottrup ◽  
J. Ørnsholt ◽  
D. Andersen
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Gastric Fistula ◽  
Adrenergic Blockade

Inhibitory effects of beta-adrenergic agonists on gastric acid secretion in dogs

1986 ◽  
Vol 251 (4) ◽  
pp. G453-G459
Author(s):  
M. H. Stevens ◽  
R. C. Thirlby ◽  
C. T. Richardson ◽  
M. A. Fredrickson ◽  
R. H. Unger ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Intravenous Infusion ◽  
Acid Output ◽  
Gastric Fistula ◽  
Adrenergic Agonists ◽  
Inhibitory Effects ◽  
Beta Adrenergic ◽  
Beta Adrenergic Agonists

We evaluated the effect of two beta-adrenergic agonists, isoproterenol (nonselective agonist) and terbutaline (selective beta 2-agonist), on gastric acid secretion stimulated by intravenous pentagastrin, bethanechol, or histamine in dogs with gastric fistulas. Intravenous infusion of isoproterenol or terbutaline inhibited pentagastrin-stimulated acid secretion to a significantly greater extent than they inhibited bethanechol- or histamine-stimulated acid secretion. For example, isoproterenol (12 micrograms X kg-1 X h-1) reduced mean pentagastrin-, bethanechol-, and histamine-stimulated acid output by 86, 63, and 14%, respectively. Percent inhibition of acid secretion with terbutaline (30 micrograms X kg-1 X h-1) averaged 60, 17, and 24% for pentagastrin, bethanechol, and histamine, respectively. Terbutaline also inhibited pentagastrin-stimulated acid secretion from vagally denervated fundic pouches in a dose-related manner. Plasma somatostatin-like immunoreactivity was significantly higher during infusion of terbutaline plus pentagastrin than during infusion of pentagastrin alone. However, an intravenous infusion of 0.3 microgram X kg-1 X h-1 somatostatin-14 had no effect on pentagastrin-stimulated acid secretion from the gastric fistula, even though this infusion increased plasma somatostatin-like immunoreactivity to the same extent as terbutaline plus pentagastrin infusion. Thus the amount of somatostatin released during terbutaline infusion was not sufficient to explain the inhibition of pentagastrin-stimulated acid secretion observed.

TRH in dorsal vagal complex mediates acid response to excitation of raphe pallidus neurons in rats

1993 ◽  
Vol 265 (5) ◽  
pp. G880-G886 ◽  
Author(s):  
H. Yang ◽  
G. Ohning ◽  
Y. Tache
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Kainic Acid ◽  
Gastric Fistula ◽  
Dorsal Vagal Complex ◽  
Gastric Function ◽  
Physiological Relevance ◽  
Raphe Pallidus

The role of thyrotropin-releasing hormone (TRH) in the dorsal vagal complex (DVC) in the acid response to excitation of raphe pallidus neurons was investigated in urethan-anesthetized rats with gastric fistula. Kainic acid (0.19 microgram/30 nl) microinjected into the raphe pallidus stimulated gastric acid secretion. The response was prevented by vagotomy. A specific polyclonal TRH antibody, 8964, was raised and characterized (50% inhibitory dose for TRH was 80 pg/ml at an antibody final dilution of 1:10(5)). The TRH antibody injected intracisternally blocked the acid response to intracisternal TRH, but not that of the TRH analogue RX-77368. The TRH antibody (0.33, 0.65, or 1.3 micrograms.100 nl-1.site-1) microinjected bilaterally into the DVC prevented dose dependently by 31, 60, and 76%, respectively, the increase in acid secretion induced by kainic acid injected into the raphe pallidus. The TRH antibody (1.3 microgram/site) microinjected into medullary sites outside of the DVC had no effect. These data indicate that excitation of raphe pallidus neurons induces a vagal-dependent stimulation of gastric acid secretion that is mediated by endogenous TRH in the DVC. TRH neurons in the raphe pallidus projecting to the DVC may have a physiological relevance in the vagal regulation of gastric function.

Effect of GABA on basal and vagally mediated gastric acid secretion and hormone release in dogs

1988 ◽  
Vol 254 (5) ◽  
pp. G723-G731
Author(s):  
R. C. Thirlby ◽  
M. H. Stevens ◽  
A. J. Blair ◽  
F. Petty ◽  
I. L. Crawford ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Blood Brain Barrier ◽  
Gaba Receptors ◽  
Gaba Receptor ◽  
Receptor Agonist ◽  
Acid Output ◽  
Gastric Fistula ◽  
Heidenhain Pouch

To stimulate peripheral gamma-aminobutyric acid (GABA) receptors, GABA, which does not cross the blood-brain barrier, was administered to dogs with vagally innervated gastric fistulas at intravenous doses of 0, 0.66, 2, 6, 18, and 54 micrograms.kg-1.min-1. Mean gastric acid output increased from zero basally to 3.0 +/- 1.4 mmol/h during infusion of 54 micrograms.kg-1.min-1 GABA. Plasma somatostatin-like immunoreactivity decreased significantly below basal levels during infusion of 54 micrograms.kg-1.min-1 GABA (P less than 0.05). To stimulate central nervous system GABA receptors as well as peripheral GABA receptors, progabide, a GABA-receptor agonist, which readily crosses the blood-brain barrier, was injected intravenously. Mean acid output was 3.5 +/- 1.3 mmol/h after 20 mg/kg progabide and 0.6 +/- 0.5 mmol/h after its vehicle (P less than 0.05). Basal serum gastrin concentration increased significantly after progabide injection. Acid output during insulin-induced hypoglycemia was inhibited 59% by 30 mg/kg intravenous progabide. Progabide infusion also diminished or abolished circulating gastrin, somatostatin, and pancreatic polypeptide responses during insulin-induced hypoglycemia (P less than 0.05). Further studies were performed in dogs with a gastric fistula and a vagally denervated Heidenhain pouch to confirm that GABA-receptor stimulation affects acid secretion via peripheral pathways. Intravenous injection of baclofen (0.5 mg/kg), a GABAB-receptor agonist, increased acid secretion significantly from the gastric fistula and the Heidenhain pouch. These studies suggest that GABA may play a role in regulating gastric acid secretion and gastrointestinal and pancreatic endocrine function by both central and peripheral mechanisms.

Inhibition of Pentagastrin-Stimulated Gastric Acid Secretion by Upper Intestinal Hyperosmolality in Chronic Gastric Fistula Rats

Digestion ◽  
1982 ◽  
Vol 24 (3) ◽  
pp. 183-189 ◽  
Author(s):  
M. Mogard ◽  
S. Emås ◽  
G. Nylander ◽  
B. Wallin ◽  
C. Wallin
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Gastric Fistula

Pharmacological evidence for histamine H3 receptor in the control of gastric acid secretion in cats

1991 ◽  
Vol 260 (4) ◽  
pp. G631-G635 ◽  
Author(s):  
A. Bado ◽  
F. Hervatin ◽  
M. J. Lewin
Keyword(s):  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Gastric Fistula ◽  
Gastric Acid Output ◽  
H2 Receptor Antagonist ◽  
H2 Receptor ◽  
H3 Receptor

We investigated the possible involvement of H3 receptor in the control of gastric acid secretion in the conscious cat provided with a gastric fistula [main stomach (MS)] and a denervated Heidenhain pouch (HP). Intravenous infusion of the selective H3 agonist (R)-alpha-methylhistamine at 3, 10, and 30 nmol.kg-1.h-1 induced a dose-related inhibition of pentagastrin-stimulated gastric acid output. Maximal inhibition in MS (48 +/- 3%, P less than 0.01) and HP (36 +/- 5%, P less than 0.01) was obtained with 30 nmol.kg-1.h-1. This dose also significantly inhibited peptone meal-induced gastric acid output by 38 +/- 4 and 46 +/- 8% (P less than 0.01) in MS and HP, respectively. These inhibitions were completely prevented by 10 nmol.kg-1.h-1 iv of the selective H3 receptor antagonist thioperamide. On the other hand, (R)-alpha-methylhistamine was without any effect on histamine-stimulated gastric acid output, whereas thioperamide produced a slight but not significant increase of this output in contrast to the H2 receptor antagonist ranitidine, which showed a strong inhibitory effect. These findings suggest that pentagastrin- or meal-induced gastric acid secretion involves an H3 receptor pharmacologically distinct from the H2 receptor.

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