Is nitric oxide involved in the tonic inhibition of central sympathetic outflow in humans?
Is nitric oxide involved in the tonic inhibition of central sympathetic outflow in humans?
复制标题
一氧化氮是否参与人类中枢交感神经流出的强直性抑制？
DOI：
10.1161/01.hyp.24.4.439
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Victor,RG
中科院分区：
文献类型：
--
作者：
Hansen,J;Jacobsen,TN;Victor,RG
最近在实验动物中的研究提出了神经元型一氧化氮是紧张性抑制交感血管收缩剂从脑干流出的信号转导通路的重要组成部分的概念。为了确定这一概念是否可以扩展到人类交感神经流出的控制，我们在静脉输注一氧化氮合酶抑制剂NG-单甲基-L-精氨酸（L-NMMA）（3.6至6.7 mg/kg）期间记录了健康人类受试者的肌肉交感神经活动（微电极，腓神经）。主要的新发现是，静脉注射L-NMMA时，平均动脉压升高（10 +/- 2 mm Hg，P < .05），而心率和交感神经活动分别降低（P < .05）10 +/- 2次/分钟和61 +/-5%。这些反射性降低与用苯乙醯胺（一种内部血管收缩剂对照）升高血压时产生的反射性降低无法区分。当L-NMMA诱导的血压升高在实验上减弱以最小化压力反射激活时，交感神经活动和心率不变。此外，在静脉输注L-精氨酸（323至513 mg/kg）以增加一氧化氮合成的过程中，平均动脉压降低（12 +/- 2 mm Hg，P < .05），但心率和交感神经活动分别增加（P < .05）11 +/- 2次/分钟和98 +/-27%。因此，我们在人体中的实验没有为一氧化氮参与中枢交感神经流出的紧张性抑制的新概念提供支持。
Recent studies in experimental animals have advanced the concept that neuronal nitric oxide is an important component of the signal transduction pathways that tonically restrain sympathetic vasoconstrictor outflow from the brain stem. To determine whether or not this concept can be extended to the control of sympathetic outflow in humans, we recorded muscle sympathetic nerve activity (microelectrodes, peroneal nerve) in healthy human subjects during intravenous infusion of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA) (3.6 to 6.7 mg/kg). The major new finding is that during intravenous L-NMMA mean arterial pressure increased (10 +/- 2 mm Hg, P < .05), whereas heart rate and sympathetic nerve activity decreased (P < .05) by 10 +/- 2 beats per minute and 61 +/- 5%, respectively. These reflex decreases were indistinguishable from those produced when blood pressure was increased comparably with phenylephrine, an internal vasoconstrictor control. When the L-NMMA-induced increase in blood pressure was attenuated experimentally to minimize baroreflex activation, sympathetic nerve activity and heart rate were unchanged. Furthermore, during infusion of L-arginine (323 to 513 mg/kg IV) to increase nitric oxide synthesis, mean arterial pressure decreased (12 +/- 2 mm Hg, P < .05), but heart rate and sympathetic nerve activity increased (P < .05) by 11 +/- 2 beats per minute and 98 +/- 27%, respectively. Thus, our experiments in humans provide no support for the emerging concept that nitric oxide is involved in the tonic restraint of central sympathetic outflow.