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[慢性交感神经去神经支配中去甲肾上腺素-H3摄取的逆向跨突触调节]

[Reverse transsynaptic regulation of noradrenaline-H3 uptake in chronic sympathetic denervation].

作者信息

Kurbanova G D, Manukhin B N

出版信息

Fiziol Zh SSSR Im I M Sechenova. 1983 Sep;69(9):1164-9.

PMID:6641995
Abstract

A change in the functional state of adrenoreceptors in conditions of chronic sympathectomy with guanethidine produces constant spontaneous release of chemical factors regulating the intensity of neuronal uptake of noradrenaline-H3 by an adrenergic neuron. In the first two months when adrenoreceptors experience constant deficit of excitation, the factors are released increasing by half the neuronal uptake of noradrenaline-H3 in atrium and v. deferens. Some increase of NA concentration in peripheral organs during the 3rd month seemingly creates conditions providing for constant activation of sensitized adrenoreceptors which results in the release of factors inhibiting the rate of NA--H3 uptake in atrium by 65%, in v. deferens by 38%. The release from effector cell of chemical agents regulating the intensity of neuronal NA uptake, is one of the local peripheral mechanisms regulating the adrenergic transmitter process.

摘要

在用胍乙啶进行慢性交感神经切除的情况下,肾上腺素能受体功能状态的改变会导致调节肾上腺素能神经元对去甲肾上腺素 - H3摄取强度的化学因子持续自发释放。在最初两个月,当肾上腺素能受体持续缺乏兴奋时,这些因子的释放量增加,使心房和输精管中去甲肾上腺素 - H3的神经元摄取量增加一半。第三个月外周器官中去甲肾上腺素浓度的一些增加似乎创造了条件,使致敏的肾上腺素能受体持续激活,这导致抑制心房中去甲肾上腺素 - H3摄取率65%、输精管中摄取率38%的因子释放。效应细胞释放调节神经元去甲肾上腺素摄取强度的化学物质,是调节肾上腺素能递质过程的局部外周机制之一。

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