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目的 探讨新型γ-氨基丁酸(GABA)受体拮抗剂左旋一叶萩碱中枢升压作用的GABA能机制与肾交感神经紧张性的关系。方法 在麻醉大鼠侧脑室注射左旋一叶萩碱(1-Sec),记录动脉血压(AP)及肾交感神经放电(RSND)。结果 (1)1-Sec和CABA_A受体拮抗剂荷包牡丹碱(Bic)均可引起RSND增加、AP升高。并呈一定剂量-效应关系;GABA_A受体激动剂蝇蕈醇(Mus)和GABA_B受体激动剂巴氯酚(Bac)使RSND减少、AP降低;(2)1-Sec既能拮抗Mus(GABA)、又能拮抗Bac引起的“交感抑制和降压反应”。结论 前脑室周部位存在“GABA能抑制机制”,1-Sec解除了GABA对交感心血管中枢的紧张性抑制,使交感神经系统传出活动增强,因而产生升压作用;1-Sec可能是一种非选择性的GABA受体拮抗剂。
Objective To investigate the relationship between the GABAergic mechanism of the central pressor action of the novel γ-aminobutyric acid (GABA) receptor antagonist levophylline and renal sympathetic tone. Methods Left cervicaline (1-Sec) was injected into the lateral ventricle of anesthetized rats to record arterial blood pressure (AP) and renal sympathetic nerve discharge (RSND). Results (1) Both 1-Sec and CABA_A receptor antagonist bicuculline (Bic) increased RSND and increased AP. It showed a dose-response relationship; GABA_A receptor agonist muscimol (Mus) and GABA_B receptor agonist baclofen (Bac) decreased RSND and AP decreased; (2) 1-Sec could antagonize Mus (GABA) ), and can antagonize the “sympathetic inhibition and hypotensive response” caused by Bac. Conclusion There is a “GABAergic inhibitory mechanism” in the periventricular region of the forebrain. 1-Sec relieves the stress-induced inhibition of the sympathetic cardiovascular center by GABA and enhances the sympathetic nervous system’s efferent activity, resulting in a boosting effect; 1-Sec may be a A non-selective GABA receptor antagonist.