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钠摄入量与内皮损伤生物标志物和代谢失调有关。

Sodium Intake Is associated With Endothelial Damage Biomarkers and Metabolic Dysregulation.

机构信息

Departamento de Endocrinología, Pontificia Universidad Católica de Chile, Santiago, Chile.

Millennium Institute on Immunology and Immunotherapy (IMII), Santiago, Chile.

出版信息

Am J Hypertens. 2018 Sep 11;31(10):1127-1132. doi: 10.1093/ajh/hpy097.

DOI:10.1093/ajh/hpy097
PMID:29917063
Abstract

BACKGROUND

Mounting evidence has associated high sodium (HS) intake with hypertension, cardiovascular disease, and stroke. We investigated whether HS intake modulates the parameters of endothelial damage, inflammation, and oxidative stress.

METHODS

We used a cross-sectional study design including 223 Chilean subjects (6.9-65.0 years old). We measured aldosterone, renin activity, cortisol, cortisone, adiponectin, leptin, hsCRP, interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α), plasminogen activator inhibitor type 1 (PAI-1), metalloproteinase (MMP)-9 and MMP-2 activity, and malondialdehyde. Sodium and creatinine were measured in 24-hour urine samples. The subjects were divided by sodium intake, high sodium (HS): ≥150 mEq/day, n = 118, and adequate sodium (AS): <150 mEq/day, n = 105.

RESULTS

We observed a positive correlation between urinary sodium excretion and blood pressure (r = 0.1669, P = 0.0124 for systolic and r = 0.2416, P = 0.0003 for diastolic), glycemia (r = 0.2660, P < 0.0001), and triglycerides (r = 0.1604, P = 0.0175) and a highly significant correlation between sodium excretion and PAI-1 (r = 0.2701, P < 0.0001). An inverse correlation was observed between urinary sodium and HDL-cholesterol (r = -0.2093, P = 0.0018) and adiponectin (r = -0.2679, P < 0.0001). In a linear regression model, urinary sodium excretion remained significantly associated with PAI-1 values even after adjusting for age, gender, and BMI. The HS group had higher blood pressure, glycemia, HOMA-IR, atherogenic index of plasma, and PAI-1 values than the group with AS intake.

CONCLUSIONS

HS intake is associated with endothelial damage (high PAI-1) and metabolic dysregulation. On the other hand, inflammation and oxidative stress parameters are not modified by sodium intake.

摘要

背景

越来越多的证据表明,高钠(HS)摄入与高血压、心血管疾病和中风有关。我们研究了高钠摄入是否调节内皮损伤、炎症和氧化应激的参数。

方法

我们使用了一项包括 223 名智利受试者(6.9-65.0 岁)的横断面研究设计。我们测量了醛固酮、肾素活性、皮质醇、皮质酮、脂联素、瘦素、hsCRP、白细胞介素 6(IL-6)、肿瘤坏死因子-α(TNF-α)、纤溶酶原激活物抑制剂 1(PAI-1)、金属蛋白酶(MMP)-9 和 MMP-2 活性以及丙二醛。24 小时尿液样本中测量了钠和肌酐。根据钠摄入量将受试者分为高钠(HS)组:≥150mEq/天,n=118;和适量钠(AS)组:<150mEq/天,n=105。

结果

我们观察到尿钠排泄与血压(收缩压 r = 0.1669,P = 0.0124;舒张压 r = 0.2416,P = 0.0003)、血糖(r = 0.2660,P < 0.0001)和甘油三酯(r = 0.1604,P = 0.0175)呈正相关,与 PAI-1 呈高度显著相关(r = 0.2701,P < 0.0001)。尿钠与 HDL-胆固醇(r = -0.2093,P = 0.0018)和脂联素(r = -0.2679,P < 0.0001)呈负相关。在线性回归模型中,即使在调整年龄、性别和 BMI 后,尿钠排泄仍与 PAI-1 值显著相关。HS 组的血压、血糖、HOMA-IR、血浆致动脉粥样硬化指数和 PAI-1 值均高于 AS 组。

结论

高钠摄入与内皮损伤(高 PAI-1)和代谢失调有关。另一方面,钠摄入不改变炎症和氧化应激参数。

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