Water deprivation does not augment sympathetic or pressor responses to sciatic afferent nerve stimulation in rats or to static exercise in humans.
Water deprivation does not augment sympathetic or pressor responses to sciatic afferent nerve stimulation in rats or to static exercise in humans.
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缺水不会增强大鼠对坐骨传入神经刺激或人类静态运动的交感神经或升压反应。
DOI：
10.1152/japplphysiol.00005.2019
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发表时间：
2019
期刊：
影响因子：
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通讯作者：
Farquhar,WilliamB
中科院分区：
文献类型：
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作者：
Watso,JosephC;Babcock,MatthewC;Robinson,AustinT;Migdal,KamilaU;Wenner,MeganM;Stocker,SeanD;Farquhar,WilliamB
过量的食盐摄入可使中枢交感神经网络兴奋，这可能与高钠血症有关。血浆高钠血症也发生在缺水（WD）之后。本研究的目的是验证WD诱导高钠血症，从而增强交感神经和升压反应的交感神经兴奋性刺激在大鼠和人类的假设。交感神经活动（SNA）和动脉血压（ABP）的反应坐骨神经传入刺激（2-20 Hz）和化学刺激的头端腹外侧延髓（RVLM）在大鼠WD后48小时进行了评估，并与正常水合对照大鼠（CON）进行比较。在一个平行的随机交叉人体实验（n= 13健康的年轻人），交感神经（microneurography）和升压（photoplethysmography）的静态运动反应进行了比较之间的16小时WD和CON条件。在大鼠中，血浆[Na+]在WD中显著高于CON [136 ± 2 vs. 144 ± 2（SD）mM，P< 0.01]，但坐骨传入神经刺激引起肾SNA [5 Hz，174 ± 34 vs. 169 ± 49%（SD），n= 6-8]和平均ABP [5 Hz，21 ± 6 vs. 18 ± 7（SD mmHg，n= 6-8]。RVLM注射谷氨酸也产生了类似的增加SNA和ABP在WD与CON大鼠。在人体中，WD增加血清[Na+] [140.6 ± 2.1 vs. 142.1 ± 1.9 mM（SD），P= 0.02]，但不增加交感神经[肌肉SNA：较基线变化（Δ）6 ± 7 vs. 5 ± 7（SD）爆发/分钟，P= 0.83]或平均ABP [Δ 12 ± 5 vs. 11 ± 8（SD）mmHg，P= 0.73;所有结果的WD与CON]在运动的最后一分钟的反应。这些研究结果表明，尽管引起相对高钠血症，WD不增加交感神经或升压反应坐骨神经传入刺激大鼠或静态exercise in humans.NEW & NOTEWORTHY过量的饮食中的盐摄入量兴奋中枢交感神经网络，这可能与血浆高钠血症。血浆高钠血症也发生在缺水（WD）之后。我们试图确定是否血浆高钠血症/高渗透压引起的WD增强交感神经和升压反应交感神经兴奋性刺激。我们的研究结果表明，WD不增加交感神经或升压反应坐骨神经刺激大鼠或静态运动在人类。
Excess dietary salt intake excites central sympathetic networks, which may be related to plasma hypernatremia. Plasma hypernatremia also occurs following water deprivation (WD). The purpose of this study was to test the hypothesis that WD induces hypernatremia and consequently augments sympathetic and pressor responses to sympathoexcitatory stimuli in rats and humans. Sympathetic nerve activity (SNA) and arterial blood pressure (ABP) responses to sciatic afferent nerve stimulation (2–20 Hz) and chemical stimulation of the rostral ventrolateral medulla (RVLM) were assessed in rats after 48 h of WD and compared with normally hydrated control rats (CON). In a parallel randomized-crossover human experiment (n= 13 healthy young adults), sympathetic (microneurography) and pressor (photoplethysmography) responses to static exercise were compared between 16-h WD and CON conditions. In rats, plasma [Na+] was significantly higher in WD versus CON [136 ± 2 vs. 144 ± 2 (SD) mM,P< 0.01], but sciatic afferent nerve stimulation produced similar increases in renal SNA [5 Hz, 174 ± 34 vs. 169 ± 49% (SD),n= 6–8] and mean ABP [5 Hz, 21 ± 6 vs. 18 ± 7 (SD mmHg,n= 6–8]. RVLM injection ofl-glutamate also produced similar increases in SNA and ABP in WD versus CON rats. In humans, WD increased serum [Na+] [140.6 ± 2.1 vs. 142.1 ± 1.9 mM (SD),P= 0.02] but did not augment sympathetic [muscle SNA: change from baseline (Δ) 6 ± 7 vs. 5 ± 7 (SD) bursts/min,P= 0.83] or mean ABP [Δ 12 ± 5 vs. 11 ± 8 (SD) mmHg,P= 0.73; WD vs. CON for all results] responses during the final minute of exercise. These findings suggest that despite eliciting relative hypernatremia, WD does not augment sympathetic or pressor responses to sciatic afferent stimulation in rats or to static exercise in humans.NEW & NOTEWORTHYExcess dietary salt intake excites central sympathetic networks, which may be related to plasma hypernatremia. Plasma hypernatremia also occurs following water deprivation (WD). We sought to determine whether plasma hypernatremia/hyperosmolality induced by WD augments sympathetic and pressor responses to sympathoexcitatory stimuli. Our findings suggest that WD does not augment sympathetic or pressor responses to sciatic afferent nerve stimulation in rats or to static exercise in humans.