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:
The American journal of physiology
影响因子:
--
通讯作者:
M. Lewin
M. Lewin
中科院分区:
--
文献类型:
--
作者:
André Bado;F. Hervatin;M. Lewin

文献摘要

被引文献

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我们研究了 H3 受体在具有胃瘘 [主胃 (MS)] 和去神经海德汉袋 (HP) 的清醒猫中可能参与胃酸分泌控制的情况。静脉输注 3、10 和 30 nmol.kg-1.h-1 选择性 H3 激动剂 (R)-α-甲基组胺可诱导对五肽胃泌素刺激的胃酸排出量产生剂量相关的抑制。使用 30 nmol.kg-1.h-1 获得了对 MS(48 +/- 3%,P 小于 0.01)和 HP(36 +/- 5%,P 小于 0.01)的最大抑制。在 MS 和 HP 中,该剂量还显着抑制蛋白胨餐诱导的胃酸排出,分别达 38 +/- 4 和 46 +/- 8%(P 小于 0.01)。这些抑制作用可被 10 nmol.kg-1.h-1 iv 选择性 H3 受体拮抗剂硫过酰胺完全阻止。另一方面,(R)-α-甲基组胺对组胺刺激的胃酸排出量没有任何影响,而与H2受体拮抗剂雷尼替丁相比,硫过酰胺对胃酸排出量产生轻微但不显着的增加,后者显示出强烈的抑制作用。这些发现表明,五肽胃泌素或膳食诱导的胃酸分泌涉及药理学上不同于 H2 受体的 H3 受体。
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.