Melatonin and Salt on Blood Vessel Function

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  • sponsor
    University of Delaware
Updated on 3 October 2022
Accepts healthy volunteers


Increased dietary sodium causes increases in oxidative stress and damages blood vessels. Americans eat more than the recommended amount of sodium. Melatonin is a powerful endogenous antioxidant that has reduced oxidative stress levels in clinical and healthy populations. This study will investigate whether melatonin can attenuate the negative effects of sodium on blood vessels.


Americans consume on average double the recommended amount of sodium established by organizations such as the American Heart Association and the Dietary Guidelines for Americans. Excess dietary sodium damages the inside of our blood vessels in a process known as endothelial dysfunction. This reduces the ability of blood vessels to dilate as much. This type of dysfunction can lead to the development of cardiovascular disease. Animal and human studies have identified one potential mechanism linking high sodium consumption and endothelial dysfunction; that is oxidative stress. Furthermore, high dietary sodium consumption has been shown to increase blood pressure reactivity in animal studies. Melatonin is a powerful endogenous antioxidant that has reduced oxidative stress levels in clinical and healthy populations. Melatonin has been shown to attenuate sympathetic responses, but research is limited. Whether supplementation of melatonin can offset the deleterious effects of a high sodium diet is unknown. Thus, the purpose of this study is to investigate the effect of melatonin supplementation compared to a placebo on markers of oxidative stress and blood vessel function in healthy young adults that consume a 10-day high sodium diet. Our hypotheses are that: 1) melatonin will reduce oxidative stress levels and restore blood vessel function and 2) melatonin will reduce the sympathetic nerve response to high sodium consumption.

Condition Cardiovascular Risk Factor
Treatment Placebo, Melatonin
Clinical Study IdentifierNCT04325191
SponsorUniversity of Delaware
Last Modified on3 October 2022

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