钾摄入量增加对肾素-血管紧张素-醛固酮系统及皮下阻力动脉的影响：一项随机交叉研究。

Effect of increased potassium intake on the renin-angiotensin-aldosterone system and subcutaneous resistance arteries: a randomized crossover study.

作者信息

Dreier Rasmus, Abdolalizadeh Bahareh, Asferg Camilla L, Hölmich Lisbet R, Buus Niels H, Forman Julie L, Andersen Ulrik B, Egfjord Martin, Sheykhzade Majid, Jeppesen Jørgen L

机构信息

Department of Medicine, Amager Hvidovre Hospital in Glostrup, University of Copenhagen, Glostrup, Denmark.

Department of Clinical Physiology, Nuclear Medicine and PET, Rigshospitalet Glostrup, University of Copenhagen, Glostrup, Denmark.

出版信息

Nephrol Dial Transplant. 2020 Jun 29. doi: 10.1093/ndt/gfaa114.

DOI:10.1093/ndt/gfaa114

PMID:32596729

Abstract

BACKGROUND

Increased potassium intake lowers blood pressure (BP) in hypertensive patients. The underlying mechanism is not fully understood but must be complex because increased potassium intake elevates circulating concentrations of the BP-raising hormone aldosterone.

METHODS

In a randomized placebo-controlled crossover study in 25 normotensive men, we investigated the effect of 4 weeks of potassium supplement (90 mmol/day) compared with 4 weeks of placebo on the renin-angiotensin-aldosterone system (RAAS), urine composition and 24-h ambulatory BP. Vascular function was also assessed through wire myograph experiments on subcutaneous resistance arteries from gluteal fat biopsies.

RESULTS

Higher potassium intake increased urinary potassium excretion (144.7 ± 28.7 versus 67.5 ± 25.5 mmol/24-h; P < 0.0001) and plasma concentrations of potassium (4.3 ± 0.2 versus 4.0 ± 0.2 mmol/L; P = 0.0002), renin {mean 16 [95% confidence interval (CI) 12-23] versus 11 [5-16] mIU/L; P = 0.0047}, angiotensin II [mean 10.0 (95% CI 6.2-13.0) versus 6.1 (4.0-10.0) pmol/L; P = 0.0025] and aldosterone [mean 440 (95% CI 336-521) versus 237 (173-386) pmol/L; P < 0.0001]. Despite RAAS activation, systolic BP (117.6 ± 5.8 versus 118.2 ± 5.2 mmHg; P = 0.48) and diastolic BP (70.8 ± 6.2 versus 70.8 ± 6.3 mmHg; P = 0.97) were unchanged. In the wire myograph experiments, higher potassium intake did not affect endothelial function as assessed by acetylcholine [logarithmically transformed half maximal effective concentration (pEC50): 7.66 ± 0.95 versus 7.59 ± 0.85; P = 0.86] and substance P (pEC50: 8.42 ± 0.77 versus 8.41 ± 0.89; P = 0.97) or vascular smooth muscle cell reactivity as assessed by angiotensin II (pEC50: 9.01 ± 0.86 versus 9.02 ± 0.59; P = 0.93) and sodium nitroprusside (pEC50: 7.85 ± 1.07 versus 8.25 ± 1.32; P = 0.25) but attenuated the vasodilatory response of retigabine (pEC50: 7.47 ± 1.16 versus 8.14 ± 0.90; P = 0.0084), an activator of Kv7 channels.

CONCLUSIONS

Four weeks of increased potassium intake activates the RAAS in normotensive men without changing BP and this is not explained by improved vasodilatory responses ex vivo.

摘要

背景

高血压患者增加钾摄入量可降低血压（BP）。其潜在机制尚未完全明确，但必定很复杂，因为增加钾摄入量会提高升血压激素醛固酮的循环浓度。

方法

在一项针对25名血压正常男性的随机安慰剂对照交叉研究中，我们调查了4周钾补充剂（90 mmol/天）与4周安慰剂相比，对肾素 - 血管紧张素 - 醛固酮系统（RAAS）、尿液成分和24小时动态血压的影响。还通过对臀肌活检获取的皮下阻力动脉进行线式肌动描记实验来评估血管功能。

结果

较高的钾摄入量增加了尿钾排泄（144.7±28.7对67.5±25.5 mmol/24小时；P<0.0001）以及血浆钾浓度（4.3±0.2对4.0±0.2 mmol/L；P = 0.0002）、肾素{平均值16[95%置信区间（CI）12 - 23]对11[5 - 16] mIU/L；P = 0.0047}、血管紧张素II[平均值10.0（95% CI 6.2 - 13.0）对6.1（4.0 - 10.0）pmol/L；P = 0.0025]和醛固酮[平均值440（95% CI 336 - 521）对从237（173 - 386）pmol/L；P<0.0001]。尽管RAAS被激活，但收缩压（117.6±5.8对118.2±5.2 mmHg；P = 0.48）和舒张压（70.8±6.2对70.8±6.3 mmHg；P = 0.97）未发生变化。在线式肌动描记实验中，较高的钾摄入量未影响通过乙酰胆碱[对数转换的半数最大效应浓度（pEC50）：7.66±0.95对7.59±0.85；P = 0.86]和P物质（pEC50：8.42±0.77对8.41±0.89；P = 0.97）评估的内皮功能，也未影响通过血管紧张素II（pEC50：9.01±0.86对9.02±0.59；P = 0.93）和硝普钠（pEC50：7.85±1.07对8.25±1.32；P = 0.25）评估的血管平滑肌细胞反应性，但减弱了瑞替加滨（一种Kv7通道激活剂）的血管舒张反应（pEC50：7.47±1.16对8.14±0.90；P = 0.0084）。