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Randomized Controlled Trial
. 2023 Dec;11(24):e15896.
doi: 10.14814/phy2.15896.

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

Affiliations
Randomized Controlled Trial

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

Macarena Ramos Gonzalez et al. Physiol Rep. 2023 Dec.

Abstract

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.

Keywords: NIRS; brachial artery FMD; melatonin; oxidative stress; sodium.

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Figures

FIGURE 1
FIGURE 1
Macrovascular function assessed via brachial artery flow‐mediated dilation (FMD) at the end of the high sodium diet plus placebo condition (HSD + PL) and at the end of the high sodium diet plus melatonin condition (HSD + MEL). (a) Relative FMD; (b) Shear rate area under the curve (AUC) to peak reached during reactive hyperemia. n = 22. Data were analyzed using paired t‐tests and are presented as both the average and individual data points.
FIGURE 2
FIGURE 2
Microvascular function assessed via near‐infrared spectroscopy during vascular occlusion test (NIRS‐VOT) at the end of the high sodium diet plus placebo condition (HSD + PL) and at the end of the high sodium diet plus melatonin condition (HSD + MEL). (a), Slope 2, also known as reperfusion slope; (b) Tissue saturation index area under the curve (TSI AUC). n = 22. Data were analyzed using paired t‐tests and are presented as both the average and individual data points.
FIGURE 3
FIGURE 3
Reactive oxygen species (ROS) at the end of the high sodium diet plus placebo condition (HSD + PL) and the high sodium diet plus melatonin condition (HSD + MEL). (a) Nitroxide concentration; (b) total number of free radicals. n = 21. Data were analyzed using paired t‐tests and are presented as both the average and individual data points.

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