首页> 美国卫生研究院文献>The Journal of Physiology >Sympathetic nerve traffic correlates with the release of nitric oxide in humans: implications for blood pressure control.
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Sympathetic nerve traffic correlates with the release of nitric oxide in humans: implications for blood pressure control.

机译:交感神经运输与人体内一氧化氮的释放有关:对血压控制的影响。

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摘要

1. Resting human sympathetic vasoconstrictor traffic displays large reproducible inter-individual differences which are similar in nerves to muscle, heart and kidney. In spite of this there is no correlation between levels of blood pressure and sympathetic traffic. To test the hypothesis that the pressor effect of the vasoconstrictor activity is counteracted by a circulating dilating factor we measured muscle nerve sympathetic activity (MSA) and an indicator of nitric oxide release (plasma nitrate) in healthy young males. 2. Sympathetic activity was recorded with the microneurographic technique in the peroneal nerve and a forearm venous plasma sample was obtained in twenty-one normotensive males aged 21-28 years. Plasma nitrate was analysed by gas chromatography and mass spectrometry. 3. There was a positive linear correlation between the plasma nitrate concentration and the strength of MSA both when the nerve activity was expressed as bursts per minute and bursts per 100 heart beats (r = 0.51, P = 0.02 and r = 0.46, P = 0.04, respectively). 4. The data suggest that the stronger the sympathetic activity the higher the release of the dilating substance, nitric oxide. This would be expected to counteract vasoconstrictor effects of the nerve traffic and thereby contribute to the lack of relationship between resting levels of MSA and blood pressure. We speculate that altered coupling between sympathetic traffic and nitric oxide release may cause abnormal peripheral resistance, e.g. in hypertension.
机译:1.休息的人的交感性血管收缩药的流量显示出可重现的个体差异,在神经方面与肌肉,心脏和肾脏相似。尽管如此,血压水平和交感神经量之间没有相关性。为了检验这一假设,即血管收缩剂活性的加压作用被循环的扩张因​​子所抵消,我们在健康的年轻男性中测量了肌肉神经交感活性(MSA)和一氧化氮释放指标(硝酸血浆)。 2.用微神经造影技术记录了腓神经的交感神经活动,并从21名年龄在21-28岁的血压正常男性中获得了前臂静脉血浆样品。硝酸血浆通过气相色谱和质谱分析。 3.当神经活动表示为每分钟爆发次数和每100次心跳爆发次数时,血浆硝酸盐浓度与MSA强度之间呈线性正相关(r = 0.51,P = 0.02和r = 0.46,P =分别为0.04)。 4.数据表明,交感活性越强,扩张物质一氧化氮的释放就越高。预期这将抵消神经交通的血管收缩作用,从而导致MSA静息水平与血压之间缺乏联系。我们推测,交感神经通量与一氧化氮释放之间的偶联改变可能会引起异常的外周阻力,例如在高血压。

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