scholarly journals Measurement of gastric acid secretion in isolated gastric mucosa of the rat: Effects of secretagogues and inhibitors including cyclic adenosine monophosphate related agents and an H2-receptor antagonist.

1977 ◽  
Vol 25 (8) ◽  
pp. 1934-1940 ◽  
Author(s):  
KAZUO WATANABE ◽  
HIROSHI Y. WATANABE ◽  
YOSHIAKI GOTO ◽  
YOKO KARIYA
Keyword(s):  
Gastric Mucosa ◽  
Acid Secretion ◽  
Receptor Antagonist ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
H2 Receptor Antagonist ◽  
H2 Receptor

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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