H2受体阻断对组氨酸脱羧酶的激活作用：作用机制
Activation of histidine decarboxylase by H2-receptor blockade: mechanism of action.
作者信息
Häkanson R, Hedenbro J, Liedberg G, Rehfeld J F, Stadil F
出版信息
Br J Pharmacol. 1975 Jan;53(1):127-30. doi: 10.1111/j.1476-5381.1975.tb07339.x.
Abstract
1 Treatment with histamine H2-receptor antagonists, which inhibit basal acid secretion was found to activate rat stomach histidine decarboxylase. At the same time the serum gastrin concentration was greatly increased. 2 In antrectomized rats neither the enzyme activity nor the serum gastrin concentration was affected by the treatment. 3 In analogy with previous observations on other inhibitors of acid secretion we suggest that the H2-receptor antagonists stimulate gastrin release through their effect on acid secretion and that the raised serum gastrin level is responsible for the enzyme activation.
摘要
- 人们发现，使用抑制基础酸分泌的组胺H2受体拮抗剂进行治疗会激活大鼠胃组织中的组氨酸脱羧酶。与此同时，血清胃泌素浓度大幅升高。2. 在切除胃窦的大鼠中，该治疗对酶活性和血清胃泌素浓度均无影响。3. 与先前对其他酸分泌抑制剂的观察结果类似，我们认为H2受体拮抗剂通过其对酸分泌的作用刺激胃泌素释放，而升高的血清胃泌素水平是酶激活的原因。
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本文引用的文献
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2
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Eur J Pharmacol. 1970 Sep 1;12(1):94-103. doi: 10.1016/0014-2999(70)90033-6.
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