Effect of Increased Potassium Intake on Adrenal Cortical and Cardiovascular Responses to Angiotensin II: A Randomized Crossover Study.
Effect of Increased Potassium Intake on Adrenal Cortical and Cardiovascular Responses to Angiotensin II: A Randomized Crossover Study.
复制标题
增加钾摄入量对肾上腺皮质和心血管对血管紧张素 II 反应的影响：随机交叉研究。
DOI：
10.1161/jaha.120.018716
复制
发表时间：
2021-05-04
影响因子：
5.4
通讯作者：
Jeppesen JL
中科院分区：
文献类型：
--
作者：
Dreier R;Andersen UB;Forman JL;Sheykhzade M;Egfjord M;Jeppesen JL
增加钾的摄入量可以降低高血压患者的血压，但增加钾的摄入量也会升高血压升高激素醛固酮的血浆浓度。除了其已充分描述的肾脏效应外，醛固酮还被认为具有血管效应，通过存在于内皮和血管平滑肌细胞中的盐皮质激素受体起作用，尽管盐皮质激素受体非依赖性作用也被认为涉及。为了进一步了解钾摄入量增加和钾刺激的高醛固酮症对人体心血管系统的影响，我们在25名健康血压正常的男性中进行了一项随机安慰剂对照双盲交叉研究，其中4周补钾治疗（90 mmol/天）与4周安慰剂治疗进行了比较。在每个治疗期结束时，我们测量了血浆中的钾和醛固酮，并进行了血管紧张素II（AngII）输注实验，在此期间，我们评估了血浆中的醛固酮反应。在AngII输注期间，还使用ECG、阻抗心动图、手指体积描记术（血压监测）和多普勒超声监测血流动力学。研究表明，较高的钾摄入量会增加血浆钾（平均值±SD，4.3±0.2 vs 4.0±0.2 mmol/L; P=0.0002）和醛固酮（中位数[四分位距]，440 [336-521] vs 237 [173-386] pmol/L; P<0.0001），并且基于重复测量的线性混合模型，增加钾摄入量可增强AngII刺激的醛固酮分泌（P=0.0020）。相比之下，钾和安慰剂给药后对AngII的血流动力学反应（血压、总外周阻力、心输出量和肾动脉血流量）相似。在健康血压正常的男性中，增加钾摄入可增强AngII刺激的醛固酮分泌，而不影响全身心血管血流动力学。EudraCT编号：2013 - 004460 - 66; URL：https://www.ClinicalTrials.gov;唯一标识符：NCT 02380157。
Increased potassium intake lowers blood pressure in patients with hypertension, but increased potassium intake also elevates plasma concentrations of the blood pressure‐raising hormone aldosterone. Besides its well‐described renal effects, aldosterone is also believed to have vascular effects, acting through mineralocorticoid receptors present in endothelial and vascular smooth muscle cells, although mineralocorticoid receptors‐independent actions are also thought to be involved. To gain further insight into the effect of increased potassium intake and potassium‐stimulated hyperaldosteronism on the human cardiovascular system, we conducted a randomized placebo‐controlled double‐blind crossover study in 25 healthy normotensive men, where 4 weeks treatment with a potassium supplement (90 mmol/day) was compared with 4 weeks on placebo. At the end of each treatment period, we measured potassium and aldosterone in plasma and performed an angiotensin II (AngII) infusion experiment, during which we assessed the aldosterone response in plasma. Hemodynamics were also monitored during the AngII infusion using ECG, impedance cardiography, finger plethysmography (blood pressure‐monitoring), and Doppler ultrasound. The study showed that higher potassium intake increased plasma potassium (mean±SD, 4.3±0.2 versus 4.0±0.2 mmol/L; P=0.0002) and aldosterone (median [interquartile range], 440 [336–521] versus 237 [173–386] pmol/L; P<0.0001), and based on a linear mixed model for repeated measurements, increased potassium intake potentiated AngII‐stimulated aldosterone secretion (P=0.0020). In contrast, the hemodynamic responses (blood pressure, total peripheral resistance, cardiac output, and renal artery blood flow) to AngII were similar after potassium and placebo. Increased potassium intake potentiates AngII‐stimulated aldosterone secretion without affecting systemic cardiovascular hemodynamics in healthy normotensive men. EudraCT Number: 2013‐004460‐66; URL: https://www.ClinicalTrials.gov; Unique identifier: NCT02380157.