Riphagen Ineke J, Gijsbers Lieke, van Gastel Maatje D A, Kema Ido P, Gansevoort Ron T, Navis Gerjan, Bakker Stephan J L, Geleijnse Johanna M
aTop Institute Food and Nutrition, Wageningen, the NetherlandsbDepartment of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, the NetherlandscDivision of Human Nutrition, Wageningen University, Wageningen, the NetherlandsdDepartment of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands*Ineke J. Riphagen and Lieke Gijsbers contributed equally.
J Hypertens. 2016 Feb;34(2):215-20. doi: 10.1097/HJH.0000000000000786.
Lifestyle measures including dietary sodium restriction and increased potassium intake are recognized to lower blood pressure (BP). Potassium was found to be effective in reducing BP at higher levels of sodium intake, but to have little effect when sodium intake is restricted. The humoral mechanisms underlying these sodium intake dependent effects of potassium are unknown. We investigated the effects of potassium supplementation on top of a fully controlled sodium-restricted diet on markers of osmoregulation and volume regulation.
In this post-hoc analysis, we included 35 (pre)hypertensive individuals participating in a randomized, double-blind, placebo-controlled crossover trial. Individuals received capsules containing sodium [3.0 g (130 mmol)/day], potassium [2.8 g (72 mmol)/day], or placebo for three four-week periods. Linear mixed-effect models were used to estimate the effects of potassium supplementation compared with placebo. Skewed data were ln-transformed before analysis.
Increased potassium intake was associated with a significant decrease in 24-h BP (-3.6/-1.6 mmHg). Furthermore, we found a significant decrease in ln MR-proANP [-0.08 (95% confidence interval -0.15, -0.01) pmol/l, P = 0.03] and significant increases in 24-h heart rate [2.5 (0.9, 4.0) bpm, P = 0.002], ln plasma copeptin [0.11 (0.01, 0.20) pmol/l, P = 0.02], ln renin [0.34 (0.08, 0.60) μIU/ml, P = 0.01], and ln aldosterone [0.14 (0.07, 0.22) nmol/l, P < 0.001] compared with placebo.
We found that potassium has BP-lowering effects during sodium restriction. These BP-lowering effects, however, seem mitigated by several counter regulatory mechanisms (i.e. increased secretion of vasopressin, stimulation of RAAS, and increased heart rate) that were activated to maintain volume homeostasis and counterbalance the decrease in BP.
包括限制饮食中钠摄入和增加钾摄入在内的生活方式措施被认为可降低血压（BP）。研究发现，在钠摄入量较高时，钾对降低血压有效，但在钠摄入受限的情况下，钾的作用甚微。钾的这些依赖于钠摄入的效应背后的体液机制尚不清楚。我们研究了在完全控制的限钠饮食基础上补充钾对渗透调节和容量调节标志物的影响。
在这项事后分析中，我们纳入了35名（预）高血压个体，他们参与了一项随机、双盲、安慰剂对照的交叉试验。个体在三个为期四周的时间段内分别服用含钠[3.0克（130毫摩尔）/天]、钾[2.8克（72毫摩尔）/天]的胶囊或安慰剂。使用线性混合效应模型来估计补充钾与安慰剂相比的效果。分析前对偏态数据进行自然对数转换。
钾摄入量增加与24小时血压显著降低（-3.6 / -1.6毫米汞柱）相关。此外，我们发现与安慰剂相比，N末端B型利钠肽原的自然对数显著降低[-0.08（95%置信区间-0.15，-0.01）皮摩尔/升，P = 0.03]，24小时心率显著增加[2.5（0.9，4.0）次/分钟 bpm，P = 0.002]，血浆 copeptin 的自然对数显著增加[0.11（0.01，0.20）皮摩尔/升，P = 0.02]，肾素的自然对数显著增加[0.34（0.08，0.60）微国际单位/毫升，P = 0.01]，醛固酮的自然对数显著增加[0.14（0.07，0.22）纳摩尔/升，P < 0.001]。
我们发现，在限钠期间钾具有降低血压的作用。然而，这些降血压作用似乎被几种反调节机制（即抗利尿激素分泌增加、肾素 - 血管紧张素 - 醛固酮系统激活和心率增加）所减弱，这些机制被激活以维持容量稳态并抵消血压的下降。
