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首页> 外文期刊>Circulation journal >Reduction of nitric oxide-mediated γ-amino butyric acid release in rostral ventrolateral medulla is involved in superoxide-induced sympathoexcitation of hypertensive rats
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Reduction of nitric oxide-mediated γ-amino butyric acid release in rostral ventrolateral medulla is involved in superoxide-induced sympathoexcitation of hypertensive rats

机译：减少一氧化氮介导的脊髓外侧髓质髓质中的γ-氨基丁酸释放涉及超氧化物诱导的高血压大鼠同情瘤

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Background: The rostral ventrolateral medulla (RVLM) in the brainstem is responsible for regulation of the sympathetic nervous system. In the RVLM, nitric oxide (NO)-mediated y-amino butyric acid (GABA) is a major sympatho-inhibitory amino acid neurotransmitter and superoxide is a major sympathoexcitatory factor. In this study, we investigated whether or not NO-mediated GABA release is involved in superoxide-induced sympathoexcitation in the RVLM of hypertensive rats. Methods and Results: For our model hypertensive rats with sympathoexcitation, we used stroke-prone spontaneously hypertensive rats (SHRSP). GABA levels in the RVLM were measured by in vivo microdialysis. Microinjection of tempol, a superoxide scavenger, into the RVLM decreased arterial pressure (AP), heart rate (HR), and renal sympathetic nerve activity (RSNA) with an increase in GABA release in the RVLM. Microinjection of NG-mono-methyl-L-arginine (L-NMMA), an NO synthase inhibitor, into the RVLM increased AP, HR, and RSNA with a decrease in GABA release in the RVLM. Prior microinjection of L-NMMA into the RVLM attenuated the tempol-induced changes in AP, HR, RSNA, and GABA release in the RVLM. Microinjection of bicuculline, a GABA receptor blocker, into the RVLM attenuated the tempol- and L-NMMA-induced changes in AP, HR, and RSNA. Conclusions: The findings suggest that reduction of NO-mediated GABA release in the RVLM is partly involved in superoxide-induced sympathoexcitation of SHRSP.
机译：背景：脑干中的rostral ventrolateral medulla（Rvlm）负责调节交感神经系统。在RVLM中，一氧化氮（NO）介导的Y-氨基丁酸（GABA）是主要的同情抑制氨基酸神经递质和超氧化物是主要的同性鉴定因子。在这项研究中，我们研究了无介导的GABA释放是否参与超氧化物诱导的高血压大鼠RVLM中的同情泌尿症。方法和结果：对于具有同情血症的模型高血压大鼠，我们使用中风易于自发性高血压大鼠（SHRSP）。 RVLM中的GABA水平是通过体内微透析测量的。 Tempol，超氧化物清除剂的显微注射，进入RVLM中的动脉压（AP），心率（HR）和肾交感神经活性（RSNA），随着RVLM中的GABA释放增加。 Ng-单甲基-1-精氨酸（L-NMMA），NO合酶抑制剂的显微注射，进入RVLM增加的AP，HR和RSNA，在RVLM中的GABA释放减少。 L-NMMA的先前显微注射到RVLM中衰减了RVLM中AP，HR，RSNA和GABA释放的Tempol诱导的变化。 BiCulline，GABA受体阻断剂的微注射，进入RVLM，衰减了AP，HR和RSNA的Tempol和L-NMMA诱导的变化。结论：调查结果表明，RVLM中无介导的GABA释放的减少部分参与超氧化物诱导的SHRP的同情。

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