Bragulat E, de la Sierra A, Antonio M T, Jiménez W, Coca A
Hypertension Unit, Department of Internal Medicine, IDIBAPS (Institut d'Investigacions Biomédiques August Pi i Sunyer), Hospital Clinic, University of Barcelona, Villarroel 170, 08036-Barcelona, Spain.
Clin Sci (Lond). 2001 Jul;101(1):73-8.
The aim of the present study was to evaluate the effects of the level of salt intake on endothelium-derived factors in a group of patients with essential hypertension. A group of 50 patients with essential hypertension who had never been treated for the condition were placed on a low-sodium (50 mmol/day), low-nitrate (400 micromol/day) diet, which was supplemented, in a single-blind fashion, with placebo tablets for the first 7 days and then with NaCl tablets (200 mmol/day) for a further 7 days (total sodium intake 250 mmol/day). At the end of both periods, 24-h ambulatory blood pressure monitoring was performed. In addition, plasma levels and 24-h urinary excretion of nitrites plus nitrates and cGMP were measured, along with plasma levels of endothelin. A high salt intake promoted significant decreases in plasma levels of nitrites plus nitrates (from 41.0+/-2.1 to 32.8+/-1.8 nmol/ml; P<0.001), 24-h urinary nitrate excretion (from 417+/-36 to 334+/-37 micromol/24 h; P=0.045) and plasma endothelin levels (from 5.6+/-0.3 to 4.6+/-0.3 pg/ml; P=0.007). The plasma concentration and 24-h urinary excretion of cGMP were not altered significantly by a high salt intake. We did not find any relationship between endothelium-derived products and 24-h mean blood pressure, at either low or high salt intakes, or between changes induced by the high-salt diet. A high salt intake also induced significant decreases in plasma renin activity, angiotensin II and aldosterone, and a significant increase in atrial natriuretic peptide. We conclude that a high salt intake decreases the plasma concentration and urinary excretion of nitrates and plasma levels of endothelin in patients with essential hypertension, suggesting that the level of salt intake may affect endothelial cell function. However, these alterations are not correlated with changes in blood pressure induced by the high salt intake.
本研究的目的是评估盐摄入量水平对一组原发性高血压患者内皮衍生因子的影响。将50例从未接受过该疾病治疗的原发性高血压患者置于低钠(50 mmol/天)、低硝酸盐(400 μmol/天)饮食中,在单盲方式下,前7天补充安慰剂片,然后再连续7天补充氯化钠片(200 mmol/天)(总钠摄入量250 mmol/天)。在两个阶段结束时,进行24小时动态血压监测。此外,测量血浆中亚硝酸盐加硝酸盐和cGMP的水平以及24小时尿排泄量,同时测量血浆内皮素水平。高盐摄入促使血浆中亚硝酸盐加硝酸盐水平显著降低(从41.0±2.1降至32.8±1.8 nmol/ml;P<0.001)、24小时尿硝酸盐排泄量降低(从417±36降至334±37 μmol/24小时;P=0.045)以及血浆内皮素水平降低(从5.6±0.3降至4.6±0.3 pg/ml;P=0.007)。高盐摄入对cGMP的血浆浓度和24小时尿排泄量没有显著影响。我们未发现低盐或高盐摄入时内皮衍生产物与24小时平均血压之间存在任何关系,也未发现高盐饮食引起的变化之间存在关系。高盐摄入还导致血浆肾素活性、血管紧张素II和醛固酮显著降低,心房利钠肽显著升高。我们得出结论,高盐摄入会降低原发性高血压患者血浆中硝酸盐的浓度和尿排泄量以及血浆内皮素水平,这表明盐摄入量可能会影响内皮细胞功能。然而,这些改变与高盐摄入引起的血压变化无关。