Pharmacological evidence for histamine H3 receptor in the control of gastric acid secretion in cats.
Pharmacological evidence for histamine H3 receptor in the control of gastric acid secretion in cats.
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组胺 H3 受体控制猫胃酸分泌的药理学证据。
DOI:
10.1152/ajpgi.1991.260.4.g631
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发表时间:
1991
期刊:
影响因子:
--
通讯作者:
M. Lewin
中科院分区:
文献类型:
--
作者:
André Bado;F. Hervatin;M. Lewin
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.