Melatonin supplementation does not alter vascular function or oxidative stress in healthy normotensive adults on a high sodium diet.

Melatonin supplementation does not alter vascular function or oxidative stress in healthy normotensive adults on a high sodium diet.
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DOI:
10.14814/phy2.15896
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发表时间:
2023-12
影响因子:
2.5
通讯作者:
--
中科院分区:
其他
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高钠饮食 (HSD) 可导致血管功能障碍,部分原因是活性氧 (ROS) 增加。褪黑激素可减少健康和临床人群中的活性氧,并可能改善血管功能。目的是确定 HSD 期间补充褪黑激素对血管功能和 ROS 的影响。我们假设,与单独 HSD 相比,在 HSD 期间补充褪黑激素可以改善血管功能并降低 ROS 水平。 27 名参与者(13 岁/14 岁,26.7±2.9 岁,BMI:23.6±2.0kg/m2,血压:110±9/67±7mmHg)被随机分配至为期 10 天的 HSD (6900 毫克钠/天)每天补充 10 毫克褪黑激素 (HSD + MEL) 或安慰剂 (HSD + PL)。肱动脉血流介导的扩张,衡量大血管功能(HSD + PL:7.1 ± 3.8%;HSD + MEL:6.7 ± 3.4%;p = 0.59)和组织氧合指数(TSI)再灌注率,衡量微血管反应性, (HSD + PL:0.21 ± 0.06%/s;HSD + MEL:0.21 ± 0.08%/s;p = 0.97)和TSI曲线下面积(HSD + PL: 199899 ± 10,863 a.u.;HSD + MEL:20315 ± 11,348 a.u.;p = 0.17)在每种条件结束时相似。硝基氧摩尔浓度(HSD + PL:7.8 × 10−5 ± 4.1 × 10−5 mol/L;HSD + MEL:8.7 × 10−5 ± 5.1 × 10−5 mol/L; p = 0.55)或自由基数(HSD + PL:8.0 × 1015 ± 4.4 × 1015;HSD + MEL:9.0 × 1015 ± 4.9 × 1015; p = 0.51)在不同条件下是不同的。在这个血压正常的年轻健康成年人样本中,服用 HSD 时,补充褪黑激素不会改变血管功能或 ROS 水平。
High sodium diets (HSD) can cause vascular dysfunction, in part due to increases in reactive oxygen species (ROS). Melatonin reduces ROS in healthy and clinical populations and may improve vascular function. The purpose was to determine the effect of melatonin supplementation on vascular function and ROS during 10 days of a HSD. We hypothesized that melatonin supplementation during a HSD would improve vascular function and decrease ROS levels compared to HSD alone. Twenty‐seven participants (13 M/14 W, 26.7 ± 2.9 years, BMI: 23.6 ± 2.0 kg/m2, BP: 110 ± 9/67 ± 7 mmHg) were randomized to a 10‐day HSD (6900 mg sodium/d) supplemented with either 10 mg of melatonin (HSD + MEL) or a placebo (HSD + PL) daily. Brachial artery flow‐mediated dilation, a measure of macrovascular function, (HSD + PL: 7.1 ± 3.8%; HSD + MEL: 6.7 ± 3.4%; p = 0.59) and tissue oxygenation index (TSI) reperfusion rate, a measure of microvascular reactivity, (HSD + PL: 0.21 ± 0.06%/s; HSD + MEL: 0.21 ± 0.08%/s; p = 0.97) and TSI area under the curve (HSD + PL: 199899 ± 10,863 a.u.; HSD + MEL: 20315 ± 11,348 a.u.; p = 0.17) were similar at the end of each condition. Neither nitroxide molarity (HSD + PL: 7.8 × 10−5 ± 4.1 × 10−5 mol/L; HSD + MEL: 8.7 × 10−5 ± 5.1 × 10−5 mol/L; p = 0.55) nor free radical number (HSD + PL: 8.0 × 1015 ± 4.4 × 1015; HSD + MEL: 9.0 × 1015 ± 4.9 × 1015; p = 0.51) were different between conditions. Melatonin supplementation did not alter vascular function or ROS levels while on a HSD in this sample of young healthy normotensive adults.