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Cited by 136Sodium Intake and HealthCardiovascular Health and Disease PreventionNitric Oxide and Endothelin Effects

High dietary sodium intake impairs endothelium-dependent dilation in healthy salt-resistant humans

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DuPont, Jennifer J., Greaney, Jody L., Wenner, Megan M., Lennon-Edwards, Shannon L., Sanders, Paul W., Farquhar, William B., Edwards, David G.·2013·Journal of Hypertension
DOI 10.1097/hjh.0b013e32835c6ca8PMC PMC4176919
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Abstract

BACKGROUND: Excess dietary sodium has been linked to the development of hypertension and other cardiovascular diseases. In humans, the effects of sodium consumption on endothelial function have not been separated from the effects on blood pressure. The present study was designed to determine if dietary sodium intake affected endothelium-dependent dilation (EDD) independently of changes in blood pressure. METHOD: Fourteen healthy salt-resistant adults were studied (9M, 5F; age 33 ± 2.4 years) in a controlled feeding study. After a baseline run-in diet, participants were randomized to a 7-day high-sodium (300-350 mmol/day) and 7-day low-sodium (20 mmol/day) diet. Salt resistance, defined as a 5 mmHg or less change in a 24-h mean arterial pressure, was individually assessed while on the low-sodium and high-sodium diets and confirmed in the participants undergoing study (low-sodium: 85 ± 1 mmHg; high-sodium: 85 ± 2 mmHg). EDD was determined in each participant via brachial artery flow-mediated dilation on the last day of each diet. RESULTS: Sodium excretion increased during the high-sodium diet (P < 0.01). EDD was reduced on the high-sodium diet (low: 10.3 ± 0.9%, high: 7.3 ± 0.7%; P < 0.05). The high-sodium diet significantly suppressed plasma renin activity (PRA), plasma angiotensin II, and aldosterone (P < 0.05). CONCLUSION: These data demonstrate that excess salt intake in humans impairs endothelium-dependent dilation independently of changes in blood pressure.

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  • Diets with sodium at or below 500 mg per day activate the renin-angiotensin-aldosterone system and raise sympathetic outflow.

    “Extremely low sodium diets (≤500mg/d) elicit activation of the renin-angiotensin-aldosterone system and stimulate sympathetic outflow.”

    From Reducing Dietary Sodium to 1000 mg per Day Reduces Neurovascular Transduction Without Stimulating Sympathetic Outflow (2019) · cites this paper as [18]

    The Methods describe a low-sodium diet of 20 mmol/day (about 460 mg/day), and the Results show higher renin activity, angiotensin II, and aldosterone on that diet than on the high-sodium diet. The paper does not report sympathetic outflow, so it does not support that part of the claim. Page numbers are unavailable in our copy. (LLM, conf=0.84)

    Experimental — accuracy not yet measured

  • The authors previously found even higher RAAS levels with a 500 mg/day sodium diet without short-term adverse effects.

    “we have previously shown even greater RAAS levels using a 500 mg/d sodium diets with no short-term adverse effects.18”

    From Reducing Dietary Sodium to 1000 mg per Day Reduces Neurovascular Transduction Without Stimulating Sympathetic Outflow (2019) · cites this paper as [18]

    The Methods (page unavailable) describe a seven-day low-sodium diet of 20 mmol/day, approximately 460 mg/day. The Results (page unavailable) report higher renin activity, angiotensin II, and aldosterone on that diet than on the high-sodium diet, with no difference in measured blood pressure. The paper does not establish the broader claim that the low-sodium diet had no short-term adverse effects. (LLM, conf=0.83)

    Experimental — accuracy not yet measured

  • Lower dietary sodium has been shown to enhance endothelial function.

    “Reduced dietary sodium has been shown to improve endothelial function,13, 17, 18, 21”

    From Reducing Dietary Sodium to 1000 mg per Day Reduces Neurovascular Transduction Without Stimulating Sympathetic Outflow (2019) · cites this paper as [18]

  • Sodium intake and RAAS activation are strongly inversely related.

    “Due to the robust inverse relation between sodium intake and RAAS activation,7, 17, 18”

    From Reducing Dietary Sodium to 1000 mg per Day Reduces Neurovascular Transduction Without Stimulating Sympathetic Outflow (2019) · cites this paper as [18]

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Authors
DuPont, J. J., Greaney, J. L., Wenner, M. M., Lennon-Edwards, S. L., Sanders, P. W., Farquhar, W. B., & Edwards, D. G.
Affiliations
  • University of Delaware (US)
  • Yale University (US)
  • University of Alabama at Birmingham (US)
Corresponding author
  • Farquhar, William B.
  • Edwards, David G.
ORCID
Venue
Journal of Hypertension
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2013-03
Volume
31
Issue
3
Pages
530-536
ISSN
0263-6352 (ISSN-L)
DOI
10.1097/hjh.0b013e32835c6ca8
PMC
PMC4176919
OpenAlex
W2021280090
Semantic Scholar
bbdecf08cd20b612cdbc982191c34ea4917e928b
Cited by
135
References
52
Citations by year
2026: 7 · 2025: 6 · 2024: 2 · 2023: 11 · 2022: 14 · 2021: 7 · 2020: 15 · 2019: 19 · 2018: 7 · 2017: 11 · 2016: 9 · 2015: 13 · 2014: 8 · 2013: 3 · 2012: 1
FWCI
7.47
Type
journal article
Language
en
Open access
Locations
  • Journal of Hypertension (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Heart, Lung, and Blood Institute (R01HL104106)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK046199, P30DK079337)
  • National Center for Research Resources (P20RR016472)
Topics
  • Health Sciences › Nursing › Nutrition and Dietetics › Sodium Intake and Health
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
sodium intake, endothelium-dependent dilation, endothelial function, hypertension, brachial artery flow-mediated dilation, plasma renin activity, angiotensin II, aldosterone, sodium excretion, sodium restriction
MeSH terms
Adult, Endothelium, Vascular, Female, Humans, Male, Sodium, Vasodilation

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