Differential sympathetic nerve responses to nitric oxide synthase inhibition in anesthetized rats.

Differential sympathetic nerve responses to nitric oxide synthase inhibition in anesthetized rats.
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麻醉大鼠对一氧化氮合酶抑制的不同交感神经反应。

DOI:
10.1152/ajpregu.1995.269.4.r807
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发表时间:
1995
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Kenney,MJ
Kenney,MJ
中科院分区:
--
文献类型:
--
作者:
Hirai,T;Musch,TI;Morgan,DA;Kregel,KC;Claassen,DE;Pickar,JG;Lewis,SJ;Kenney,MJ

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最近的研究表明,交感神经系统与一氧化氮(NO)或亚硝基因子之间的相互作用可能是调节动脉血压的重要手段。我们研究了NO合成酶(NOS)抑制是否能调节压力感受器神经支配和去神经支配的氯醛麻醉大鼠基底交感神经放电(SND)。我们记录了给予NOS抑制剂ng -硝基- l -精氨酸甲酯(L-NAME, 20mg /kg iv)前后的平均动脉压(MAP)、肾脏SND和腰椎SND。L-NAME给药后2分钟,压力受体神经支配大鼠的MAP升高(+23 +/- 3 mmHg),而肾脏SND (-45 +/- 6%, n = 7)和腰椎SND (-35 +/- 2%, n = 6)较对照水平显著降低。这些变化在L-NAME给药后持续20分钟。在压力受体失神经大鼠中,L-NAME增加MAP (+40 +/- 6 mmHg),降低腰椎SND (n = 7) (L-NAME后20分钟比对照减少37 +/- 10%)。相比之下,给药后肾SND逐渐增加(L-NAME后20分钟+33 +/- 8%)。上述结果表明,NOS抑制可引起压力感受器失神经大鼠SND的不均匀变化,提示内源性亚硝基因子对腰椎SND具有强直兴奋作用,而对肾脏SND具有强直抑制作用。
Recent studies have suggested that the interaction between the sympathetic nervous system and nitric oxide (NO) or nitrosyl factors may be an important means by which arterial blood pressure is regulated. We investigated whether NO synthase (NOS) inhibition modulates basal sympathetic nerve discharge (SND) in baroreceptor-innervated and -denervated, chloralose-anesthetized Sprague-Dawley rats. We recorded mean arterial pressure (MAP), renal SND, and lumbar SND before and after administration of the NOS inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg iv). Two minutes after L-NAME administration in baroreceptor-innervated rats, MAP increased (+23 +/- 3 mmHg), whereas renal (-45 +/- 6%, n = 7) and lumbar (-35 +/- 2%, n = 6) SND significantly decreased from control levels. These changes persisted for up to 20 min after L-NAME administration. In baroreceptor-denervated rats, L-NAME increased MAP (+40 +/- 6 mmHg) and decreased lumbar SND (n = 7) (-37 +/- 10% from control at 20 min post-L-NAME). In contrast, renal SND progressively increased (+33 +/- 8% at 20 min post-L-NAME) from control after L-NAME administration in baroreceptor-denervated rats (n = 7). These results demonstrate that NOS inhibition can produce nonuniform changes in SND in baroreceptor-denervated rats and suggest that endogenous nitrosyl factors provide tonic excitation to lumbar SND, whereas they provide a tonic restraint to renal SND.