将D-2-氨基-7-膦酰庚酸微量注射到中脑导水管周围灰质背侧可降低对在同一部位注射谷氨酸的升压反应。
Microinjection of D-2-amino-7-phosphonoheptanoate into the dorsal periaqueductal gray matter reduces the pressor response to glutamate injected at the same site.
作者信息
Batista-Da-Silva A P, Rae G A, Carobrez A P
机构信息
Departamento de Farmacologia, Universidade Federal de Santa Catarina, Florianópolis, Brasil.
出版信息
Braz J Med Biol Res. 1990;23(8):705-8.
The current study assesses the influence of the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-7-phosphonoheptanoate (AP7) on the pressor effect of glutamate microinjected into the dorsal periaqueductal gray matter (DPAG) of urethane-anesthetized rats. Glutamate (20, 40 and 80 nmol/site) caused dose-related reproducible increases in systolic and diastolic blood pressure. Microinjection of saline into the DPAG did not alter the pressor effects of glutamate (80 nmol/site). Similar pretreatment with AP7 (2 nmol/site) significantly (P less than 0.05) attenuated the pressor effects of glutamate from +26.5 +/- 7.0 to +3.4 +/- 3.3 mmHg (systolic blood pressure). We conclude that the pressor effect of glutamate in the DPAG is mediated largely by activation of NMDA receptors.
本研究评估了N-甲基-D-天冬氨酸（NMDA）受体拮抗剂D-2-氨基-7-膦酰庚酸（AP7）对向氨基甲酸乙酯麻醉大鼠的背侧导水管周围灰质（DPAG）微量注射谷氨酸所致升压效应的影响。谷氨酸（20、40和80 nmol/部位）引起收缩压和舒张压呈剂量相关的可重复性升高。向DPAG微量注射生理盐水未改变谷氨酸（80 nmol/部位）的升压效应。用AP7（2 nmol/部位）进行类似预处理可显著（P<0.05）减弱谷氨酸的升压效应，收缩压从+26.5±7.0 mmHg降至+3.4±3.3 mmHg。我们得出结论，DPAG中谷氨酸的升压效应主要由NMDA受体激活介导。
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