Maiorov D N, Krenz N R, Krassioukov A V, Weaver L C
John P. Robarts Research Institute, University of Western Ontario, London, Canada.
Am J Physiol. 1997 Sep;273(3 Pt 2):H1266-74. doi: 10.1152/ajpheart.1997.273.3.H1266.
The neurotransmitters mediating the spinal sympathetic reflexes that initiate episodic hypertension after spinal cord injury are unknown. We examined the role of glutamatergic transmission in these reflexes by testing effects of the N-methyl-D-aspartate (NMDA)-receptor antagonist 2-amino-5-phosphonopentanoic acid (AP-5) and of the alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-receptor antagonist 2,3-dihydroxy-6-nitro-7-sulfamoylbenzoquinone (NBQX) on the reflex hypertension caused by colon distension. Antagonists were administered intrathecally in conscious rats 1-2 days (acute, n = 10) or 15-16 days (chronic, n = 14) after cord transection at the fifth thoracic segment under barbiturate anesthesia. AP-5 blocked pressor responses to intrathecal NMDA but had no effect on responses to AMPA; similarly, NBQX blocked responses to AMPA but had no effect on responses to NMDA. Before antagonist injection, colon distension increased mean arterial pressure by 24 +/- 1 mmHg (from 100 +/- 3 mmHg) and by 37 +/- 2 mmHg (from 116 +/- 3 mmHg) in the acute and chronic groups, respectively. Pretreatment with AP-5 attenuated the pressor responses by 36 and 37% in these respective groups; pretreatment with NBQX attenuated them by 34 and 31%. These data suggest that both NMDA and AMPA receptors contribute to spinal viscerosympathetic transmission and initiation of episodic hypertension in conscious spinal rats.
介导脊髓损伤后引发发作性高血压的脊髓交感反射的神经递质尚不清楚。我们通过测试N-甲基-D-天冬氨酸（NMDA）受体拮抗剂2-氨基-5-磷酸戊酸（AP-5）和α-氨基-3-羟基-5-甲基-4-异恶唑丙酸（AMPA）受体拮抗剂2,3-二羟基-6-硝基-7-氨磺酰基苯醌（NBQX）对结肠扩张引起的反射性高血压的影响，研究了谷氨酸能传递在这些反射中的作用。在巴比妥类麻醉下，于第五胸段脊髓横断后1 - 2天（急性，n = 10）或15 - 16天（慢性，n = 14），对清醒大鼠进行鞘内注射拮抗剂。AP-5阻断了对鞘内注射NMDA的升压反应，但对AMPA的反应无影响；同样，NBQX阻断了对AMPA的反应，但对NMDA的反应无影响。在注射拮抗剂之前，结肠扩张使急性组和慢性组的平均动脉压分别从100±3 mmHg升高到24±1 mmHg和从116±3 mmHg升高到37±2 mmHg。在这些相应组中，AP-5预处理分别使升压反应减弱了36%和37%；NBQX预处理使其减弱了34%和31%。这些数据表明，NMDA和AMPA受体均参与了清醒脊髓损伤大鼠的脊髓内脏交感神经传递及发作性高血压的引发。
