Bazil M K, Gordon F J
Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322.
Brain Res. 1991 Jul 26;555(1):149-52. doi: 10.1016/0006-8993(91)90871-r.
Pharmacological blockade of N-methyl-D-aspartic acid (NMDA) receptors in the spinal cord was produced by intrathecal administration of the NMDA receptor antagonist D-2-amino-7-phosphonoheptanoic acid. Blockade of spinal NMDA receptors significantly reduced arterial pressure, heart rate and sympathetic nerve activity and reduced by approximately 50% the pressor and sympathoexcitatory responses evoked by cerebral ischemia. These results indicate that NMDA receptors in the spinal cord participate in the maintenance and regulation of the sympathetic nervous system and suggest that excitatory amino acid neurotransmitters may play a role in sympathoexcitation produced by physiological activation of descending bulbospinal pathways.
通过鞘内注射N-甲基-D-天冬氨酸（NMDA）受体拮抗剂D-2-氨基-7-磷酸庚酸，实现对脊髓中NMDA受体的药理学阻断。脊髓NMDA受体的阻断显著降低了动脉血压、心率和交感神经活动，并使脑缺血诱发的升压和交感兴奋反应降低了约50%。这些结果表明，脊髓中的NMDA受体参与了交感神经系统的维持和调节，并提示兴奋性氨基酸神经递质可能在由延髓脊髓下行通路的生理激活所产生的交感兴奋中发挥作用。
