Spinal NMDA receptors mediate pressor responses evoked from the rostral ventrolateral medulla.
Spinal NMDA receptors mediate pressor responses evoked from the rostral ventrolateral medulla.
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脊髓 NMDA 受体介导延髓头端腹外侧引起的升压反应。
DOI：
10.1152/ajpheart.1991.260.1.h267
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发表时间：
1991
期刊：
影响因子：
--
通讯作者：
Gordon,FJ
中科院分区：
文献类型：
--
作者：
Bazil,MK;Gordon,FJ
这些研究调查了脊髓 N-甲基-D-天冬氨酸 (NMDA) 受体在介导 L-谷氨酸 (L-Glu) 刺激延髓头端腹外侧 (RVM) 引起的心血管反应中的作用。将 L-Glu 微量注射到尿烷麻醉大鼠的 RVM 中会增加平均动脉压 (MAP) 和心率。鞘内给予 NMDA 受体拮抗剂 D-(-)-2-氨基-7-膦酰庚酸 (D-AP-7) 或 3-((+-)-2-羧基哌嗪-4-基)-丙基-1-膦酸酯 (CPP) 可降低 MAP 和心率。胸脊髓尾段的 D-AP-7 或 CPP 阻断 NMDA 受体可显着降低 RVM 升压反应，但对诱发心动过速影响不大。将 D-AP-7 注射到头侧胸脊髓对 RVM 升压或心动过速反应没有影响。鞘内注射 D-AP-7 和 CPP 消除了鞘内 NMDA 的心血管作用，但不减少鞘内红藻氨酸或使君子酸激动剂 DL-α-氨基-3-羟基-5-甲基异恶唑-4-丙酸 (AMPA) 产生的心血管作用。这些结果表明：1) 脊髓 NMDA 受体的强直激活参与维持心脏和血管的交感神经流出，2) RVM 引起的升压反应需要脊髓 NMDA 受体的突触激活，3) 兴奋性氨基酸可能是从 RVM 下降到脊髓的升压通路的神经递质。
These studies investigated the role of spinal N-methyl-D-aspartic acid (NMDA) receptors in the mediation of cardiovascular responses evoked by L-glutamate (L-Glu) stimulation of the rostral ventrolateral medulla (RVM). Microinjections of L-Glu into the RVM of urethan-anesthetized rats increased mean arterial pressure (MAP) and heart rate. Intrathecal administration of the NMDA receptor antagonists D-(-)-2-amino-7-phosphonoheptanoic acid (D-AP-7) or 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonate (CPP) reduced MAP and heart rate. Blockade of NMDA receptors by D-AP-7 or CPP in the caudal thoracic spinal cord markedly reduced RVM pressor responses with little effect on evoked tachycardia. Administration of D-AP-7 to the rostral thoracic spinal cord had no effect on RVM pressor or tachycardic responses. Intrathecal D-AP-7 and CPP abolished the cardiovascular effects of intrathecal NMDA without reducing those produced by intrathecal kainic acid or the quisqualate agonist DL-alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA). These results indicate that 1) tonic activation of spinal NMDA receptors participates in the maintenance of sympathetic outflow to the heart and blood vessels, 2) pressor responses evoked from the RVM require synaptic activation of spinal NMDA receptors, and 3) an excitatory amino acid may be the neurotransmitter of pressor pathways descending from the RVM to the spinal cord.