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High dietary sodium intake impairs endothelium-dependent dilation in healthy salt-resistant humans
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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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“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]
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“we have previously shown even greater RAAS levels using a 500 mg/d sodium diets with no short-term adverse effects.18”
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“Reduced dietary sodium has been shown to improve endothelial function,13, 17, 18, 21”
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“Due to the robust inverse relation between sodium intake and RAAS activation,7, 17, 18”
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Metadata
- 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
- Published
- 2013-03
- Volume
- 31
- Issue
- 3
- Pages
- 530-536
- ISSN
- 0263-6352 (ISSN-L)
- 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
- FWCI
- 7.47
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- 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 (medical) › 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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