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Melatonin and Salt on Blood Vessel Function

Melatonin and Salt on Blood Vessel Function

Status
UNKNOWN
Phases
NA
Study type
Interventional
Source
ClinicalTrials.gov
Registry ID
NCT04325191
Enrollment
15
Registered
2020-03-27
Start date
2020-03-12
Completion date
2022-09-30
Last updated
2021-04-28

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Cardiovascular Risk Factor

Keywords

Vascular Health, Melatonin, Dietary Sodium, Blood Pressure

Brief summary

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.

Detailed description

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.

Interventions

DIETARY_SUPPLEMENTMelatonin

Daily consumption of a high sodium diet and melatonin for 10 days

OTHERPlacebo

aily consumption of a high sodium diet and placebo for 10 days

Sponsors

University of Delaware
Lead SponsorOTHER

Study design

Allocation
RANDOMIZED
Intervention model
CROSSOVER
Primary purpose
PREVENTION
Masking
SINGLE (Subject)

Masking description

Participant will not know if they are receiving the melatonin or placebo pills.

Intervention model description

This is a randomized crossover design trial.

Eligibility

Sex/Gender
ALL
Age
18 Years to 45 Years
Healthy volunteers
Yes

Inclusion criteria

* healthy * normal blood pressure

Exclusion criteria

* hypertension * heart disease * diabetes * kidney disease * renal impairment * cancer * obese (BMI ≥30) * sleep disorder * use of tobacco products * pregnant or breastfeeding * take any medications for the above conditions * endurance trained athletes * night shift worker * melatonin or antioxidant consumption for the previous 3 months * use of selective serotonin reuptake inhibitors

Design outcomes

Primary

MeasureTime frameDescription
Microvascular functionDay 10Assessed by Near Infrared Spectroscopy (NIRS)
Conduit artery endothelial-dependent functionDay 10Assessed by brachial artery flow mediated dilation (FMD)

Secondary

MeasureTime frameDescription
Blood pressure reactivityDay 10Assessed by the change in blood pressure during Handgrip Exercise and Cold Pressor test from baseline

Countries

United States

Contacts

Primary ContactMacarena Ramos Gonzalez, MS
macramos@udel.edu(302)831-3954
Backup ContactShannon L Lennon, PhD
slennon@udel.edu3028312798

Outcome results

None listed

Source: ClinicalTrials.gov · Data processed: Feb 4, 2026