Reply from V. A. Averina, H. G. Othmer, G. D. Fink and J. W. Osborn.
Reply from V. A. Averina, H. G. Othmer, G. D. Fink and J. W. Osborn.
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V. A. Averina、H. G. Othmer、G. D. Fink 和 J. W. Osborn 的答复。
DOI：
10.1113/jphysiol.2013.254607
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发表时间：
2013
期刊：
影响因子：
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通讯作者：
Osborn,JohnW
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作者：
Averina,ViktoriaA;Othmer,HansG;Fink,GregoryD;Osborn,JohnW
我们论文的目的不是要建立一个关于盐摄入量、盐排泄量和动脉压之间关系的综合数学模型，而是指出这些变量之间的实验和临床可观察到的关系可以在不止一组生理假设下得到解释。氯化钠排泄的调节相当复杂，涉及许多已知的和显然尚未发现的因素，其中动脉压只是其中之一（Reinhardt & Seeliger, 2000; Seeliger et al. 2004; Bie, 2009）。我们感谢 Judge 和 Dorrington 博士非常正确的观察，即血管紧张素水平的变化通常会响应不同的盐摄入量而发生，并且由此产生的对肾脏钠排泄的影响并未纳入模型中。在比我们提出的模型稍微更先进的模型中，可以通过适当调整达到钠平衡的时间常数（方程（6）中的τSE）来轻松解释这一点。然而，他们的观点并没有否定这样一个事实：即使血管紧张素 II 水平被“钳制”（Cowley & Skelton，1991；Seeliger 等，2004），由于控制钠排泄的其他强大因素（其中之一是动脉压）的作用，钠平衡最终还是会实现。还值得注意的是，血浆血管紧张素 II 水平在每日盐摄入量极低时达到最低点（Kjolby 等，2005），因此血管紧张素 II 的变化不能解释在每日钠摄入量较高时（当今大多数人群的典型情况）轻松实现钠平衡。因此，我们仍然相信，对于动脉压和肾钠排泄之间常见的关系，存在多种可能的生理学解释。
The intent of our paper was not to formulate a comprehensive mathematical model of the relationship between salt intake, salt excretion and arterial pressure, but rather to point out that the experimentally and clinically observable relationships between these variables can be explained under more than one set of physiological assumptions. The regulation of sodium chloride excretion is quite complex and involves many known and apparently yet-to-be-discovered factors of which arterial pressure is only one (Reinhardt & Seeliger, 2000; Seeliger et al. 2004; Bie, 2009). We thank Drs Judge and Dorrington for their quite correct observation that alterations in angiotensin levels would normally occur in response to different salt intakes, and that the resulting influence on renal sodium excretion is not incorporated in the model. In a slightly more developed model than the one we presented this could easily be accounted for by appropriate adjustments of the time constant for reaching sodium balance (τSE in our eqn (6)). However, their point does not invalidate the fact that sodium balance is ultimately achieved even when angiotensin II levels are ‘clamped’(Cowley & Skelton, 1991; Seeliger et al. 2004) due to the operation of other powerful factors that control sodium excretion (one of which is arterial pressure). It is also worth noting that plasma angiotensinII levels reach their nadir at surprising low daily salt intakes (Kjolby et al. 2005), and thus changes in angiotensin II cannot account for the ready achievement of sodium balance at higher daily sodium intakes (typical of most human populations today). Thus we remain convinced that there are multiple possible physiological explanations for the commonly observed relationships between arterial pressure and renal sodium excretion.