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延髓头端腹外侧区在中枢介导的升压反应中的作用。

Role of rostral ventrolateral medulla in centrally mediated pressor responses.

作者信息

Kiely J M, Gordon F J

机构信息

Department of Pharmacology, Emory University School of Medicine, Atlanta, Georgia 30322.

出版信息

Am J Physiol. 1994 Oct;267(4 Pt 2):H1549-56. doi: 10.1152/ajpheart.1994.267.4.H1549.

DOI:10.1152/ajpheart.1994.267.4.H1549
PMID:7943401
Abstract

The region of the rostral ventrolateral medulla (RVLM) plays an important role in central nervous system regulation of cardiovascular function. The initial purpose of these studies was to determine whether synaptic activation of excitatory amino acid (EAA) receptors in the RVLM might mediate central pressor responses. Blockade of EAA receptors in the RVLM with kynurenic acid abolished pressor responses evoked by stimulation of sciatic nerve afferents but had no effect on increases in arterial pressure produced by stimulation of hypothalamic sites. To determine whether synaptic transmission in the RVLM, independent of EAA receptor activation, was a prerequisite for the production of hypothalamic pressor responses, axonal conduction and/or synaptic transmission were pharmacologically interrupted in the RVLM. Blockade of synaptic transmission with muscimol or kainic acid attenuated, but did not eliminate, hypothalamic pressor responses. Concurrent blockade of synaptic and axonal transmission in the RVLM with lidocaine produced the greatest reduction of hypothalamic pressor responses. Collectively, these results suggest that central pressor responses are not uniformly mediated by synaptic activation of neurons within the RVLM. Instead, a combination of synaptic transmission and axonal conduction within and possibly outside the region of the RVLM may be required for the production of many centrally mediated pressor responses.

摘要

延髓头端腹外侧区(RVLM)在中枢神经系统对心血管功能的调节中发挥着重要作用。这些研究的最初目的是确定RVLM中兴奋性氨基酸(EAA)受体的突触激活是否可能介导中枢性升压反应。用犬尿氨酸阻断RVLM中的EAA受体会消除由刺激坐骨神经传入纤维引起的升压反应,但对刺激下丘脑部位所产生的动脉血压升高没有影响。为了确定RVLM中的突触传递(独立于EAA受体激活)是否是产生下丘脑升压反应的先决条件,在RVLM中对轴突传导和/或突触传递进行了药理学阻断。用蝇蕈醇或 kainic 酸阻断突触传递可减弱但不能消除下丘脑升压反应。用利多卡因同时阻断RVLM中的突触和轴突传递可最大程度地降低下丘脑升压反应。总体而言,这些结果表明,中枢性升压反应并非均由RVLM内神经元的突触激活介导。相反,可能需要RVLM区域内和区域外的突触传递和轴突传导共同作用才能产生许多中枢介导的升压反应。

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