Bazil M K, Gordon F J
Department of Pharmacology, Emory University School of Medicine, Atlanta, Georgia 30322.
Neuropharmacology. 1990 Oct;29(10):923-30. doi: 10.1016/0028-3908(90)90143-f.
The purpose of these studies was to investigate a potential role for N-methyl-D-aspartic acid (NMDA) receptors in the spinal cord, in the mediation of pressor responses, evoked by electrical stimulation of supraspinal pressor sites. Graded electrical stimulation (10-40 Hz) of the lateral parabrachial complex increased the mean arterial pressure by 19 to 59 mmHg, and heart rate by 4 to 12 beats/min. Intrathecal administration of the NMDA receptor antagonist D-2-amino-7-phosphonoheptanoic acid (D-AP7; 200 nmol/10 microliters) reduced the arterial pressure from 101 to 68 mmHg and heart rate from 364 to 330 beats/min. Parabrachial pressor responses were virtually eliminated after spinal administration of D-AP7 while tachycardic responses were not significantly affected. Neither intravenous administration of D-AP7 nor intrathecal infusion of vehicle had any effect on parabrachial pressor responses. Intrathecal infusion of NMDA (50 nmol) increased arterial pressure by 43 mmHg and heart rate by 53 beats/min. Intrathecal infusion of kainic acid (3 nmol) increased arterial pressure by 38 mmHg and heart rate by 54 beats/min. Intrathecal infusion of D-AP7 eliminated the pressor and tachycardic actions of NMDA, without affecting those of kainic acid. These results suggest that the maintenance of sympathetic vasomotor tone as well as the mediation of pressor responses produced by electrical stimulation of the parabrachial complex, is dependent upon synaptic activation of spinal NMDA receptors and further, that excitatory amino acid neurotransmitters in the spinal cord may play a significant role in central cardiovascular regulation.
这些研究的目的是探讨N-甲基-D-天冬氨酸（NMDA）受体在脊髓中，对由脊髓上加压部位的电刺激所诱发的升压反应的介导作用。对臂旁外侧复合体进行分级电刺激（10 - 40Hz）可使平均动脉压升高19至59mmHg，心率增加4至12次/分钟。鞘内注射NMDA受体拮抗剂D-2-氨基-7-磷酸庚酸（D-AP7；200nmol/10微升）可使动脉压从101mmHg降至68mmHg，心率从364次/分钟降至330次/分钟。脊髓注射D-AP7后，臂旁加压反应几乎完全消除，而心动过速反应未受到显著影响。静脉注射D-AP7或鞘内注射溶媒对臂旁加压反应均无任何影响。鞘内注射NMDA（50nmol）可使动脉压升高43mmHg，心率增加53次/分钟。鞘内注射 kainic 酸（3nmol）可使动脉压升高38mmHg，心率增加54次/分钟。鞘内注射D-AP7消除了NMDA的升压和心动过速作用，而不影响kainic 酸的作用。这些结果表明，交感血管运动张力的维持以及臂旁复合体电刺激所产生的升压反应的介导，依赖于脊髓NMDA受体的突触激活，并且进一步表明，脊髓中的兴奋性氨基酸神经递质可能在中枢心血管调节中起重要作用。
