根据盐摄入水平,生理盐水负荷对血压、尿钠和钾的不同急性影响:EpiSS研究。

IF 2.5
Wenjuan Peng, Yunyi Xie, Kuo Liu, Han Qi, Zheng Liu, Juan Xia, Han Cao, Chunyue Guo, Yanyan Sun, Xiaohui Liu, Bingxiao Li, Fuyuan Wen, Fengxu Zhang, Ling Zhang
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引用次数: 0

摘要

急性食盐摄入可引起血压升高。本研究旨在评估不同盐摄入水平受试者生理盐水负荷对血压的急性影响。本研究是在盐敏感性系统流行病学基线调查的基础上进行的。计算24小时尿液中钠的排泄量来估计盐的摄入水平。受试者进行急性口服生理盐水负荷试验(1 L),并纳入2019名受试者的数据进行分析。采用多元线性回归和分层分析来确定24小时尿钠(24hUNa)与血压变化之间的关系。由于生理盐水负荷,收缩压(SBP)、脉压和尿钠浓度显著升高,舒张压、心率和尿钾浓度显著降低。低盐摄入、血压正常者、老年人、男性、吸烟者和饮酒者的收缩压升高更为显著。血压升高与24hUNa呈显著的线性负剂量反应关系(β = -0.901, 95% CI: -1.253, -0.548),特别是在低盐摄入人群(β = -1.297, 95% CI: -2.338, -0.205)和高血压患者(β = -1.502, 95% CI: -2.037, -0.967)。在排除服用降糖或降压药物的患者后,负相关的影响减弱,但仍然显著。综上所述,急性盐负荷导致收缩压升高,且收缩压升高与24hUNa呈负相关。该研究表明,避免急性盐负荷对于避免急性血压变化非常重要,特别是在低盐摄入人群中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Discrepant acute effect of saline loading on blood pressure, urinary sodium and potassium according to salt intake level: EpiSS study.

Discrepant acute effect of saline loading on blood pressure, urinary sodium and potassium according to salt intake level: EpiSS study.

Discrepant acute effect of saline loading on blood pressure, urinary sodium and potassium according to salt intake level: EpiSS study.

Discrepant acute effect of saline loading on blood pressure, urinary sodium and potassium according to salt intake level: EpiSS study.

Acute dietary salt intake may cause an elevation in blood pressure (BP). The study aimed to assess the acute effect of saline loading on BP in subjects with different levels of salt intake. This study is based on the baseline survey of systemic epidemiology of salt sensitivity study. The sodium excretion in the 24-hour urine was calculated for estimating the level of salt intake. Subjects were performed an acute oral saline loading test (1 L), and data of 2019 participants were included for analyses. Multivariate linear regression and stratified analyses were performed to identify associations between 24-hour urinary sodium (24hUNa) with BP changes. Due to saline loading, systolic BP (SBP), pulse pressure, and urinary sodium concentration were significantly increased, while diastolic BP, heart rate, and urinary potassium concentration were significantly decreased. The SBP increments were more significant in subjects with lower salt intake, normotensives, elders, males, smokers, and drinkers. There was a significant linear negative dose-response association between SBP increment with 24hUNa (β = -0.901, 95% CI: -1.253, -0.548), especially in lower salt intake individuals (β = -1.297, 95% CI: -2.338, -0.205) and hypertensive patients (β = -1.502, 95% CI: -2.037, -0.967). After excluding patients who received antidiabetic or antihypertensive medicines, the effects of negative associations weakened but remained significantly. In conclusion, acute salt loading leads to an increment in SBP, and the increased SBP was negatively related with 24hUNa. This study indicated avoiding acute salt loading was important for escaping acute BP changes, especially in lower salt intake populations.

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