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重要的 GABA 能机制在 NTS 内和 SHR 的交感血压反射控制。

Important GABAergic mechanism within the NTS and the control of sympathetic baroreflex in SHR.

机构信息

Department of Physiology and Biophysics, Institute of Biomedical Science, University of São Paulo, 05508-900, São Paulo, SP, Brazil.

出版信息

Auton Neurosci. 2011 Jan 20;159(1-2):62-70. doi: 10.1016/j.autneu.2010.08.003. Epub 2010 Sep 15.

DOI:10.1016/j.autneu.2010.08.003
PMID:20837402
Abstract

Inhibitory neurotransmission has an important role in the processing of sensory afferent signals in the nucleus of the solitary tract (NTS), particularly in spontaneously hypertensive rats (SHR). In the present study, we tested the hypothesis that γ-aminobutyric acid (GABA) mediated neurotransmission within the NTS produces an inhibition of the baroreflex response of splanchnic sympathetic nerve discharge (sSND). In urethane-anesthetized, artificially ventilated and vagotomized male SHR and Wistar Kyoto (WKY) rats we compared baroreflex-response curves evoked after bilateral injections into the NTS of the GABA-A antagonist bicuculline (25pmol/50nl) or the GABA-B antagonist CGP 35348 (5nmol/50nl). Baseline MAP in SHR was higher than the WKY rats (SHR: 153±5, vs. WKY: 112±6mm Hg, p<0.05). Bilateral injection of bicuculline or CGP 35348 into the NTS induced a transient (5min) reduction in MAP (∆=-26±4 and -41±6mm Hg, respectively vs. saline ∆=+4±3mmHg, p<0.05) and sSND (∆=-21±13 and -78±7%, respectively vs. saline: ∆=+6±4% p<0.05). Analysis of the baroreceptor curve revealed a decrease in the lower plateau (43±11 and 15±5%, respectively vs. saline: 78±6%, p<0.05) and an increase in the sympathetic gain of baroreflex (6.3±0.3, 7.2±0.8% respectively vs. saline: 4.2±0.4%, p<0.05). Bicuculline or CGP35348 into the NTS in WKY rats did not change MAP, sSND and sympathetic baroreflex gain. These data indicate that GABAergic mechanisms within the NTS act tonically reducing sympathetic baroreflex gain in SHR.

摘要

抑制性神经传递在孤束核(NTS)中感觉传入信号的处理中起着重要作用,特别是在自发性高血压大鼠(SHR)中。在本研究中,我们检验了这样一个假设,即在 NTS 内γ-氨基丁酸(GABA)介导的神经传递会产生对内脏交感神经放电(sSND)的压力反射反应的抑制。在乌拉坦麻醉、人工通气和迷走神经切断的雄性 SHR 和 Wistar Kyoto(WKY)大鼠中,我们比较了双侧注射 NTS 内 GABA-A 拮抗剂荷包牡丹碱(25pmol/50nl)或 GABA-B 拮抗剂 CGP 35348(5nmol/50nl)后诱发的压力反射反应曲线。SHR 的基础 MAP 高于 WKY 大鼠(SHR:153±5,vs. WKY:112±6mmHg,p<0.05)。双侧注射 NTS 内的荷包牡丹碱或 CGP 35348 会引起 MAP 的短暂(5min)降低(分别为-26±4 和-41±6mmHg,与盐水相比分别为+4±3mmHg,p<0.05)和 sSND 的降低(分别为-21±13 和-78±7%,与盐水相比分别为+6±4%,p<0.05)。对压力感受器曲线的分析显示,下平台降低(分别为 43±11 和 15±5%,与盐水相比分别为 78±6%,p<0.05)和压力反射的交感增益增加(分别为 6.3±0.3 和 7.2±0.8%,与盐水相比分别为 4.2±0.4%,p<0.05)。在 WKY 大鼠中,将荷包牡丹碱或 CGP35348 注射到 NTS 中不会改变 MAP、sSND 和交感神经压力反射增益。这些数据表明,NTS 内的 GABA 能机制会持续地降低 SHR 的交感神经压力反射增益。

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