scholarly journals The effect of an H2-receptor antagonist on food-stimjlated acid secretion, serum gastrin, and gastric emptying in patients with duodenal ulcers. Comparison with an anticholinergic drug.

1975 ◽  
Vol 55 (3) ◽  
pp. 536-542 ◽  
Author(s):  
C T Richardson ◽  
B A Bailey ◽  
J H Walsh ◽  
J S Fordtran
Keyword(s):  
Gastric Emptying ◽  
Acid Secretion ◽  
Receptor Antagonist ◽  
Serum Gastrin ◽  
Anticholinergic Drug ◽  
H2 Receptor Antagonist ◽  
Duodenal Ulcers ◽  
H2 Receptor

Effect of histamine on rat gastric H(+)-K(+)-ATPase alpha-subunit expression

1994 ◽  
Vol 266 (3) ◽  
pp. G444-G450 ◽  
Author(s):  
A. Tari ◽  
G. Yamamoto ◽  
Y. Yonei ◽  
M. Sumii ◽  
K. Sumii ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Receptor Antagonist ◽  
Parietal Cell ◽  
Serum Gastrin ◽  
Mrna Level ◽  
Alpha Subunit ◽  
H2 Receptor Antagonist ◽  
H2 Receptor ◽  
Subunit Mrna ◽  
Subunit Expression

The H(+)-K(+)-adenosinetriphosphatase (ATPase) is expressed in the parietal cell and is responsible for acid secretion by the stomach. Histamine binds to an H2 receptor and activates adenylate cyclase and intracellular calcium concentration ([Ca2+]i) elevation, stimulating acid secretion. It has been shown that omeprazole administered to rats increases serum gastrin and transiently increases the level of mRNA for the alpha-subunit of the pump, but this increase is blocked by the presence of the H2-receptor antagonist, famotidine [A. Tari, G. Yamamoto, K. Sumii, M. Sumii, Y. Takehara, K. Haruma, G. Kajiyama, V. Wu, G. Sachs, and J. H. Walsh. Am. J. Physiol. 265 (Gastrointest. Liver Physiol. 28): G752-G758, 1993]. These observations suggest that the release of histamine induced by gastrin is essential for the increase of the expression of mRNA induced by omeprazole. Infusion of histamine at 15 mumol.kg-1.h-1 i.v. for 1 h increased the alpha-subunit mRNA level by 144 +/- 2.4% and induced a stimulated morphological appearance of the parietal cell. These changes were inhibited completely by the competitive H2-receptor antagonist famotidine, which elevated gastric pH and serum gastrin. Famotidine also reduced the level of H(+)-K(+)-ATPase mRNA compared with control animals. No change in the expression of beta-actin mRNA was observed in any group of animals. These data provide direct evidence for histamine stimulation of H(+)-K(+)-ATPase alpha-subunit gene expression by activation of the H2 receptor.

Effect of a new H2-receptor antagonist (Roxatidine acetate) on the acid secretion by isolated canine parietal cells

1989 ◽  
Vol 24 (2) ◽  
pp. 221-221
Author(s):  
Eiichi Saito ◽  
Hitomi Natomi ◽  
Masaru Kato ◽  
Kentaro Sugano ◽  
Atsuko Seki ◽  
...  
Keyword(s):  
Acid Secretion ◽  
Receptor Antagonist ◽  
Parietal Cells ◽  
H2 Receptor Antagonist ◽  
H2 Receptor ◽  
Roxatidine Acetate

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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