[在普萘洛尔同时去神经支配或阻断身体β -肾上腺素受体的背景下,器官反射性营养不良大鼠肾脏的矿皮质激素受体器官]。

Iu A Akimov, Ia I Azhipa, A A Rodionov, A I Grishchenko
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引用次数: 0

摘要

标记醛固酮与大鼠肾皮质质矿物受体和导管细胞核在不同神经营养器官供应功能障碍中的相互作用。迷走神经支配的功能障碍导致细胞质受体装置和负责醛固酮接收的导管细胞核的断裂。器官去神经支配和β -肾上腺素阻滞剂的引入可防止肾神经性营养不良的发生。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[The mineralocorticoid receptor apparatus of the kidneys in rats with reflex dystrophy of the organ against a background of simultaneous denervation or blockade of the body beta-adrenoreceptors by propranolol].

Interaction of labeled aldosterone with rat kidney mineral corticoid cytoplasm receptors and duct cell nuclei at different dysfunctions of nervous-trophic organ supply. Dysfunction of vagus innervation leads to breakage of cytoplasm receptor apparatus and duct cell nuclei that performs aldosterone reception. Organ denervation and introduction of beta-adrenoblocking agent prevents development of kidney neurogenous dystrophy.

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