Department of Kinesiology and Applied Physiology, University of Delaware, Newark, Delaware, USA.
J Hypertens. 2013 Mar;31(3):530-6. doi: 10.1097/HJH.0b013e32835c6ca8.
Excess dietary sodium has been linked to the development of hypertension and other cardiovascular diseases. In humans, the effects of sodium consumption on endothelial function have not been separated from the effects on blood pressure. The present study was designed to determine if dietary sodium intake affected endothelium-dependent dilation (EDD) independently of changes in blood pressure.
Fourteen healthy salt-resistant adults were studied (9M, 5F; age 33 ± 2.4 years) in a controlled feeding study. After a baseline run-in diet, participants were randomized to a 7-day high-sodium (300-350 mmol/day) and 7-day low-sodium (20 mmol/day) diet. Salt resistance, defined as a 5 mmHg or less change in a 24-h mean arterial pressure, was individually assessed while on the low-sodium and high-sodium diets and confirmed in the participants undergoing study (low-sodium: 85 ± 1 mmHg; high-sodium: 85 ± 2 mmHg). EDD was determined in each participant via brachial artery flow-mediated dilation on the last day of each diet.
Sodium excretion increased during the high-sodium diet (P < 0.01). EDD was reduced on the high-sodium diet (low: 10.3 ± 0.9%, high: 7.3 ± 0.7%; P < 0.05). The high-sodium diet significantly suppressed plasma renin activity (PRA), plasma angiotensin II, and aldosterone (P < 0.05).
These data demonstrate that excess salt intake in humans impairs endothelium-dependent dilation independently of changes in blood pressure.
过量的膳食钠与高血压和其他心血管疾病的发生有关。在人类中,钠摄入量对内皮功能的影响尚未与血压变化分开。本研究旨在确定膳食钠摄入量是否独立于血压变化而影响内皮依赖性舒张(EDD)。
在一项对照喂养研究中,研究了 14 名健康的耐盐成年人(9 名男性,5 名女性;年龄 33±2.4 岁)。在基线适应期饮食后,参与者被随机分配到为期 7 天的高钠(300-350mmol/天)和低钠(20mmol/天)饮食。盐抗性通过肱动脉血流介导的舒张在低钠和高钠饮食期间分别评估,并在进行研究的参与者中得到证实(低钠:85±1mmHg;高钠:85±2mmHg)。在每个饮食的最后一天,通过肱动脉血流介导的舒张来确定每个参与者的 EDD。
高钠饮食期间钠排泄增加(P<0.01)。高钠饮食时 EDD 降低(低:10.3±0.9%,高:7.3±0.7%;P<0.05)。高钠饮食显著抑制了血浆肾素活性(PRA)、血浆血管紧张素 II 和醛固酮(P<0.05)。
这些数据表明,人类过量的盐摄入会损害内皮依赖性舒张,而与血压变化无关。