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β-内啡肽对大鼠足部电击应激期间血管加压素释放的抑制作用的证据。

Evidence for inhibition by beta-endorphin of vasopressin release during foot shock-induced stress in the rat.

作者信息

Knepel W, Nutto D, Hertting G

出版信息

Neuroendocrinology. 1982;34(5):353-6. doi: 10.1159/000123327.

Abstract

This study was to ascertain the effect of naloxone and dexamethasone on vasopressin and beta-endorphin release in the rat during inescapable electric foot shock stress. Plasma vasopressin concentrations were not affected by electric foot shock in vehicle-treated rats, but were raised significantly by the stress in animals pretreated with naloxone. The stress-induced increase in plasma beta-endorphin-like immunoreactivity (beta-EI) was similar whether the rats had received naloxone or not. Plasma beta-EI consisted of equal amounts of beta-endorphin-like and beta-lipotropin-like material as revealed by gel filtration. Dexamethasone almost abolished the foot shock-induced increase in plasma beta-EI and, in the presence of dexamethasone, stress was now effective in elevating plasma vasopressin concentrations. These results are consistent with the hypothesis that beta-endorphin, released from the anterior pituitary, inhibits the release of vasopressin from the posterior lobe of the pituitary gland during foot shock-induced stress.

摘要

本研究旨在确定纳洛酮和地塞米松对大鼠在不可逃避的电足部电击应激期间血管加压素和β-内啡肽释放的影响。在给予赋形剂处理的大鼠中,血浆血管加压素浓度不受电足部电击的影响,但在用纳洛酮预处理的动物中,应激使其显著升高。无论大鼠是否接受纳洛酮,应激诱导的血浆β-内啡肽样免疫反应性(β-EI)增加相似。凝胶过滤显示,血浆β-EI由等量的β-内啡肽样物质和β-促脂素样物质组成。地塞米松几乎消除了足部电击诱导的血浆β-EI增加,并且在地塞米松存在的情况下,应激现在有效地提高了血浆血管加压素浓度。这些结果与以下假设一致:在足部电击诱导的应激期间,从垂体前叶释放的β-内啡肽抑制垂体后叶血管加压素的释放。

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