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脊髓N-甲基-D-天冬氨酸受体对室旁核控制交感神经输出的作用。

Contribution of spinal N-methyl-D-aspartic acid receptors to control of sympathetic outflow by the paraventricular nucleus.

作者信息

Porter J P

机构信息

Department of Physiology and Biophysics, University of Louisville, KY 40292.

出版信息

Brain Res Bull. 1993;32(6):653-60. doi: 10.1016/0361-9230(93)90169-c.

DOI:10.1016/0361-9230(93)90169-c
PMID:8106130
Abstract

Spinal NMDA receptors contribute to control of the cardiovascular system by the ventrolateral medulla. However, little is known about the contribution of these receptors to suprabulbar regulation of hemodynamics and sympathetic outflow. Hence, the involvement of spinal NMDA receptors in regulation of the cardiovascular system by the paraventricular nucleus (PVN) of the hypothalamus was investigated. In urethane-anesthetized rats, the change in mean arterial pressure (MAP), heart rate (HR), and renal nerve activity (RNA) produced by electrical or chemical activation of the PVN was determined before and after intrathecal administration of the NMDA receptor antagonist, 2-amino-5-phosphonovaleric acid (AP5). Intrathecal AP5 decreased resting MAP, HR, and RNA, but had no effect on the increase in RNA produced by electrical or chemical stimulation of the PVN. The pressor and renal vasoconstrictor effects resulting from electrical, but not chemical, stimulation of the PVN were significantly reduced by intrathecal AP5. These data show that much of the cardiovascular control exerted by the PVN does not depend on a spinal NMDA receptor mechanism.

摘要

脊髓N-甲基-D-天冬氨酸(NMDA)受体有助于延髓腹外侧对心血管系统的控制。然而,关于这些受体对延髓以上水平血流动力学和交感神经输出调节的作用知之甚少。因此,研究了脊髓NMDA受体在下丘脑室旁核(PVN)对心血管系统调节中的作用。在乌拉坦麻醉的大鼠中,在鞘内注射NMDA受体拮抗剂2-氨基-5-磷酸戊酸(AP5)之前和之后,测定通过电刺激或化学激活PVN所产生的平均动脉压(MAP)、心率(HR)和肾神经活动(RNA)的变化。鞘内注射AP5可降低静息MAP、HR和RNA,但对电刺激或化学刺激PVN所引起的RNA增加没有影响。鞘内注射AP5可显著降低电刺激(而非化学刺激)PVN所产生的升压和肾血管收缩效应。这些数据表明,PVN施加的大部分心血管控制并不依赖于脊髓NMDA受体机制。

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Sympathoexcitation from the rostral ventrolateral medulla is mediated by spinal NMDA receptors.来自延髓头端腹外侧的交感神经兴奋由脊髓N-甲基-D-天冬氨酸受体介导。
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