thioperamide has been researched along with tiotidine* in 2 studies
2 other study(ies) available for thioperamide and tiotidine
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Effects of N-alpha-methyl-histamine on human H(2) receptors expressed in CHO cells.
Production of N-alpha-methyl-histamine (NAMH), a histamine H(3) receptor (H3R) agonist, is reportedly promoted in Helicobacter pylori infected human gastric mucosa. NAMH was suggested to act directly on histamine H(2) receptors (H2Rs) in animals to stimulate acid secretion and to be a H2R agonist. As H2Rs and H3Rs play different roles in gastric acid secretion, it is very important to verify that NAMH is a H2R agonist.. To determine whether NAMH is a H2R agonist, as well as a H3R agonist.. We used a Chinese hamster ovary (CHO) cell line expressing human H2Rs (CHO-H2R) and control CHO cells. Expression of human H2Rs was confirmed by tiotidine binding. cAMP production in CHO-H2R and control cells in response to histamine or NAMH was measured. cAMP production in response to 10(-7) M NAMH was also measured in the presence or absence of the H2R antagonist famotidine and the H3R antagonist thioperamide.. NAMH dose dependently stimulated cAMP productions in CHO-H2R cells. This production was inhibited by famotidine but not by thioperamide. Control CHO cells were unresponsive to either histamine or NAMH. In addition, the effect of NAMH, in terms of cAMP production in CHO-H2R cells, was more potent than that of histamine-that is, with a lower EC(50) concentration and higher maximal cAMP production. Both NAMH and histamine, but not R-alpha-methyl-histamine, effectively inhibited [(3)H] tiotidine binding to CHO-H2R cells.. NAMH, which is produced in the gastric mucosa by H pylori, is a potent H2R agonist as well as a H3R agonist. Topics: Animals; CHO Cells; Cimetidine; Cricetinae; Cyclic AMP; Famotidine; Female; Histamine Agonists; Histamine Antagonists; Histamine H2 Antagonists; Methylhistamines; Ovary; Piperidines; Receptors, Histamine H2; Receptors, Histamine H3 | 2002 |
R-alpha-methylhistamine-induced inhibition of gastric acid secretion in pylorus-ligated rats via central histamine H3 receptors.
1. The effect of central H3 histamine receptor activation on gastric acid and pepsin production has been investigated in pylorus-ligated rats. 2. Intracerebroventricular injections (i.c.v.) of the selective H3 agonist, R-alpha-methylhistamine (0.5-50 nmol per rat) caused a dose-dependent inhibition of gastric acid secretion while intravenous administration (5-500 nmol per rat) was completely ineffective. 3. I.c.v. microinjections of mepyramine, tiotidine and thioperamide (51 nmol per rat), selective antagonists at H1-, H2- and H3-sites respectively, failed to modify the acid secretory response to pylorus ligation. 4. The antisecretory effect of R-alpha-methylhistamine (5 nmol per rat, i.c.v.) was selectively prevented by the H3-blocker, thioperamide (51 nmol per rat, i.c.v.), mepyramine and tiotidine pretreatment being completely inactive. 5. Unlike acid secretion, pepsin production was not significantly affected by all the tested compounds. 6. These findings provide the first pharmacological evidence that the activation of central H3 histamine receptors exerts a negative control in the regulation of gastric acid secretion in conscious pylorus-ligated rats. Topics: Animals; Cimetidine; Female; Gastric Acid; Gastric Mucosa; Histamine Agonists; Histamine Antagonists; Injections, Intraventricular; Methylhistamines; Piperidines; Pylorus; Pyrilamine; Rats; Rats, Wistar; Receptors, Histamine H3 | 1995 |