The temporal response of changes in renal sodium reabsorption during increased renal sympathetic nerve activity has not been investigated. Central hypovolemia by application of lower-body negative-pressure (LBNP) elicits baroreceptor mediated sympathetic reflexes to maintain arterial blood pressure. We hypothesized, that during 90 min LBNP, the renal sodium retention would increase rapidly, remain increased during intervention, and return to baseline immediately after end of intervention.

Methods

30 young, healthy, sodium loaded, non-obese males were exposed to −15 mmHg LBNP, −30 mmHg LBNP, −15 mmHg LBNP + renin blockade or time-control (0 mmHg LBNP) for 90 min. Urine was collected every 15 min during 90 min of intervention and 60 min of recovery to identify a possible relation between time of intervention and renal response.

Results

All intervention groups exhibited a comparable reduction in distal sodium excretion at the end of the intervention (P = 0.46 between groups; −15 mmHg: −3.1 ± 0.9 %, −30 mmHg: −2.9 ± 0.6 %, −15 mmHg + aslikiren: −1.8 ± 0.6 %). −15 mmHg+Aliskiren resulted in a slower onset, but all groups exhibited a continued reduction in sodium excretion after 1 h of recovery despite return to baseline of renin, aldosterone, diuresis and cardiovascular parameters.

Conclusion

Sympathetic stimulation for 90 min via LBNP at −30 mmHg LBNP compared to −15 mmHg did not result in a greater response in fractional Na⁺ excretion, suggesting that additional baroreceptor unloading did not cause further increases in renal sodium reabsorption. Changes in distal Na⁺ excretion were linear with respect to time (dose) of intervention, but seem to exhibit a saturation-like effect at a level around 4 %. The lack of recovery after 1 h is also a new finding that warrants further investigation.

中文翻译：

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健康男性交感神经刺激期间肾钠处理的动态变化

尚未研究肾交感神经活动增加期间肾钠重吸收变化的时间反应。通过应用下半身负压（LBNP）引起中枢低血容量，引起压力感受器介导的交感神经反射以维持动脉血压。我们假设，在 90 分钟 LBNP 期间，肾钠潴留会迅速增加，在干预期间保持增加，并在干预结束后立即恢复到基线。

方法

30 名年轻、健康、钠负荷、非肥胖男性暴露于 -15 mmHg LBNP、-30 mmHg LBNP、-15 mmHg LBNP + 肾素阻断或时间控制 (0 mmHg LBNP) 90 分钟。在干预的 90 分钟和恢复的 60 分钟期间，每 15 分钟收集一次尿液，以确定干预时间和肾脏反应之间可能的关系。

结果

所有干预组在干预结束时均表现出远端钠排泄量相当的减少（组间 P = 0.46；-15 mmHg：-3.1 ± 0.9 %，-30 mmHg：-2.9 ± 0.6 %，-15 mmHg + 阿利吉仑： −1.8 ± 0.6 %）。-15 mmHg+阿利吉仑导致起效较慢，但尽管肾素、醛固酮、利尿和心血管参数恢复到基线，但所有组在恢复1小时后均表现出钠排泄持续减少。

结论

通过LBNP在-30 mmHg下刺激交感神经90分钟，与-15 mmHg相比，LBNP并没有导致Na ⁺排泄分数的更大反应，表明额外的压力感受器卸载不会导致肾钠重吸收的进一步增加。远端 Na ⁺排泄的变化与干预时间（剂量）呈线性关系，但似乎在 4% 左右的水平表现出类似饱和的效应。1 小时后缺乏恢复也是一个值得进一步研究的新发现。