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作用于交感神经节以减弱猫下丘脑诱导的升压效应的交感抑制机制。

Sympatho-inhibitory mechanisms acting at sympathetic ganglia to attenuate hypothalamic-induced pressor effect in the cat.

作者信息

Blum B, Israeli J, Hart O, Mihiz M, Farchi M

机构信息

Department of Physiology and Pharmacology, Sackler School of Medicine, Tel Aviv University, Israel.

出版信息

Experientia. 1987 Oct 15;43(10):1106-9. doi: 10.1007/BF01956050.

Abstract

Pressor and tachycardic effects induced in the cat by stimulation of a lateral hypothalamic (LH) site, are shown to be mediated by sympathetic ganglia nicotinic receptor, and potentiated under atropine methyl nitrate sympathetic ganglia blockage. It is postulated that a sympatho-inhibitory pathway muscarinic ganglionic mechanism, co-activated by the LH stimulation, attenuates the pressor and tachycardic effects, the potentiation presumably being a manifestation of blockage of that mechanism.

摘要

刺激猫下丘脑外侧(LH)部位所诱发的升压和心动过速效应,表明是由交感神经节烟碱样受体介导的,且在硝酸甲基阿托品阻断交感神经节后会增强。据推测,LH刺激共同激活的一条交感抑制通路——毒蕈碱样神经节机制,会减弱升压和心动过速效应,这种增强可能是该机制被阻断的一种表现。

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