Microinjection of acetylcholine into cerebellar fastigial nucleus induces blood depressor response in anesthetized rats.

Microinjection of acetylcholine into cerebellar fastigial nucleus induces blood depressor response in anesthetized rats.
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将乙酰胆碱显微注射到小脑顶核可诱导麻醉大鼠的降血反应。

DOI:
10.1016/j.neulet.2016.06.063
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发表时间:
2016
影响因子:
2.5
通讯作者:
Sun Tingzhe
Sun Tingzhe
中科院分区:
医学4区
文献类型:
--
作者:
Zhang Changzheng;Luo Wen;Zhou Peiling;Sun Tingzhe

文献摘要

被引文献

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众所周知,小脑顶核(FN)参与心血管调节,并有胆碱能活动的直接证据;然而,FN中的乙酰胆碱(ACh)是否以及如何调节血压尚未被研究。在本研究中,我们分析了麻醉大鼠心房微量注射胆碱能试剂后的平均动脉压、平均动脉压最大变化、血压变化的反应时间。结果表明,乙酰胆碱具有浓度依赖性(10、30和100 mM)的降血压作用。毒蕈碱ACh (mACh)受体拮抗剂阿托品能阻断ACh介导的抑制反应,而烟碱ACh (nACh)受体拮抗剂甲胺不能。mACh受体激动剂oxotremorine M,而不是nACh受体激动剂尼古丁,以剂量依赖性的方式模拟了ach介导的血压降低(10,30和100 mM)。这些结果表明,小脑FN的胆碱能输入对全身血压调节具有抑制作用,而这种作用主要是由mACh而不是nACh受体起作用,尽管mACh受体在FN介导的血压调节中作用的确切机制仍有待阐明。
It is well known that the cerebellar fastigial nucleus (FN) is involved in cardiovascular modulation, and has direct evidence of cholinergic activity; however, whether and how acetylcholine (ACh) in the FN modulates blood pressure has not been investigated. In this study, we analyzed mean arterial pressure, maximal change in mean arterial pressure, and the reaction time of blood pressure changes after microinjection of cholinergic reagents into the FN in anesthetized rats. The results showed that ACh evoked a concentration-dependent (10, 30 and 100 mM) effect on blood pressure down-regulation. The muscarinic ACh (mACh) receptor antagonist atropine, but not the nicotinic ACh (nACh) receptor antagonist mecamylamine, blocked the ACh-mediated depressor response. The mACh receptor agonist oxotremorine M, rather than nACh receptor agonist nicotine, mimicked the ACh-mediated blood pressure decrease in a dose-dependent manner (10, 30 and 100 mM). These results indicate that cholinergic input in the cerebellar FN exerts a depressor effect on systemic blood pressure regulation, and such effects are substantially contributed by mACh rather than nACh receptors, although the precise mechanism concerning the role of mACh receptor in FN-mediated blood pressure modulation remains to be elucidated.