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首页> 外文期刊>Life sciences >Interaction between glutamatergic and nitrergic mechanisms mediating cardiovascular responses to L-glutamate injection in the diagonal band of Broca in anesthetized rats
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Interaction between glutamatergic and nitrergic mechanisms mediating cardiovascular responses to L-glutamate injection in the diagonal band of Broca in anesthetized rats

机译：介导麻醉对大鼠Broca对角带中L-谷氨酸注射的心血管反应的谷氨酸能和亚硝化机制之间的相互作用

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摘要

In a previous study, we reported depressor and bradycardiac responses after L-glutamate (L-glu) microinjection into the diagonal band of Broca (dbB) in anesthetized rats. Here, we report the glutamatergic-receptor subtype mediating the cardiovascular effects evoked by L-glu injection into the dbB and the involvement of local nitric oxide (NO) mechanisms as well as peripheral effectors. Microinjections of 100 nL Of L-glu (1, 27, 8 1, 130 or 200 nmol) into the dbB of urethane-anesthetized rats caused short-lasting depressor and bradycardiac responses. Responses were dose-related, with an ED50 of approximately 81 nmol. This dose was used in later experiments. The cardiovascular responses to L-glu in the dbB were abolished by local pretreatment (100 nL) with the selective N-methyl-D-aspartic acid (NMDA) receptor antagonist LY235959 (4 nmol) but were not affected by pretreatment with the selective non-NMDA receptor antagonist NBQX (4 nmol). Responses to L-glu in the dbB were blocked by local pretreatment with the selective neuronal NO-synthase (nNOS) inhibitor N-omega-propyl-L-arginine (NPLA, 0.04 nmol); the NO scavenger carboxy-PTIO (C-PTIO, I nmol) or the guanylate cyclase inhibitor ODQ (1 nmol). These results suggest that the microinjection Of L-glu into the dbB of urethane-anesthetized rats causes dose-related depressor and bradycardiac responses through the NMDA receptor-NO-guanylate cyclase pathway. (c) 2007 Elsevier Inc. All rights reserved.
机译：在先前的研究中，我们报道了在麻醉的大鼠中，在Broca对角带（dbB）中微注射L-谷氨酸（L-glu）后产生的抑郁和心动过缓反应。在这里，我们报告的谷氨酸能受体亚型介导L-glu注入dbB引起的心血管效应以及局部一氧化氮（NO）机制和外周效应子的参与。将100 nL L-glu（1、27、8、1、130或200 nmol）微注射到氨基甲酸酯麻醉大鼠的dbB中会引起短暂的抑郁和心动过缓反应。反应与剂量有关，ED50约为81 nmol。该剂量用于以后的实验中。用选择性N-甲基-D-天冬氨酸（NMDA）受体拮抗剂LY235959（4 nmol）进行局部预处理（100 nL）消除了dbB对L-glu的心血管反应，但不受选择性N-甲基-D-天冬氨酸预处理的影响-NMDA受体拮抗剂NBQX（4 nmol）。 dbB中对L-glu的反应被选择性神经元一氧化氮合酶（nNOS）抑制剂N-ω-丙基-L-精氨酸（NPLA，0.04 nmol）的局部预处理所阻断。 NO清除剂羧基-PTIO（C-PTIO，I nmol）或鸟苷酸环化酶抑制剂ODQ（1 nmol）。这些结果表明，将L-glu微量注入氨基甲酸酯麻醉大鼠的dbB中会通过NMDA受体-NO-鸟苷酸环化酶途径引起剂量相关的抑郁和心动过缓反应。 （c）2007 Elsevier Inc.保留所有权利。

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