Sved A F, Tsukamoto K
Department of Behavioral Neuroscience, University of Pittsburgh, PA 15260.
Brain Res. 1992 Oct 2;592(1-2):37-43. doi: 10.1016/0006-8993(92)91655-x.
Previous studies have indicated that tonic stimulation of GABAB receptors in the nucleus tractus solitarius (NTS) contributes to the regulation of arterial blood pressure (AP). The present studies examined the hypotheses that (1) tonic stimulation of GABAB receptors in the NTS provides a tonic attenuation of the baroreceptor reflex and (2) enhanced stimulation of these GABAB receptors markedly attenuates the baroreceptor reflex resulting in an increase in AP. In chloralose-anesthetized rats electrical stimulation of the aortic depressor nerve elicited frequency-dependent decreases in AP and heart rate (HR). These responses were markedly attenuated, but not eliminated, by injection of the GABAB receptor agonist baclofen into the ipsilateral NTS. In contrast, the GABAA receptor agonist muscimol completely inhibited aortic depressor nerve-evoked responses. Blockade of GABAB receptors in the NTS by local injection of CGP-35348 elicited a dose-dependent decrease in AP, and a dose-dependent blockade of the pressor response elicited by injection of baclofen into the NTS. These results support the hypothesis that GABA acts tonically on GABAB receptors in the NTS to attenuate the baroreceptor reflex, thereby contributing to the regulation of AP.
先前的研究表明,孤束核(NTS)中GABAB受体的持续性刺激有助于动脉血压(AP)的调节。本研究检验了以下假设:(1)NTS中GABAB受体的持续性刺激对压力感受器反射起到持续性减弱作用;(2)对这些GABAB受体的增强刺激会显著减弱压力感受器反射,导致动脉血压升高。在氯醛糖麻醉的大鼠中,电刺激主动脉减压神经会引起动脉血压和心率(HR)的频率依赖性降低。向同侧NTS注射GABAB受体激动剂巴氯芬可显著减弱这些反应,但并未消除。相反,GABAA受体激动剂蝇蕈醇可完全抑制主动脉减压神经诱发的反应。通过在NTS局部注射CGP-35348阻断GABAB受体,会引起动脉血压的剂量依赖性降低,以及向NTS注射巴氯芬所诱发的升压反应的剂量依赖性阻断。这些结果支持以下假设,即γ-氨基丁酸(GABA)对NTS中的GABAB受体起持续性作用,以减弱压力感受器反射,从而有助于动脉血压的调节。