Dietary sodium loading impairs microvascular function independent of blood pressure in humans: role of oxidative stress
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Key points: Pre‐clinical studies suggest that acute dietary sodium loading impairs vascular function without alterations in blood pressure; however, human data are lacking. In this study, normotensive salt‐resistant adults participated in a controlled feeding study, in which they consumed a low‐sodium diet for 1 week and a high‐sodium diet for 1 week, in random order. During each diet, microvascular function was assessed. Here we report the novel finding of sodium‐induced impairments in microvascular function independent of blood pressure in healthy adults. We additionally show that function was improved by the administration of the anti‐oxidant ascorbic acid. Therefore, in addition to its well‐known importance for blood pressure control, lowering sodium intake may have beneficial effects on microvascular function in healthy normotensive adults. Abstract Animal studies have reported dietary salt‐induced reductions in vascular function independent of increases in blood pressure (BP). The purpose of this study was to determine if short‐term dietary sodium loading impairs cutaneous microvascular function in normotensive adults with salt resistance. Following a control run‐in diet, 12 normotensive adults (31 ± 2 years) were randomized to a 7 day low‐sodium (LS; 20 mmol day−1) and 7 day high‐sodium (HS; 350 mmol day−1) diet (controlled feeding study). Salt resistance, defined as a ≤5 mmHg change in 24 h mean BP determined while on the LS and HS diets, was confirmed in all subjects undergoing study (LS: 84 ± 1 mmHg vs. HS: 85 ± 2 mmHg; P > 0.05). On the last day of each diet, subjects were instrumented with two microdialysis fibres for the local delivery of Ringer solution and 20 m m ascorbic acid (AA). Laser Doppler flowmetry was used to measure red blood cell flux during local heating‐induced vasodilatation (42°C). After the established plateau, 10 m m l‐NAME was perfused to quantify NO‐dependent vasodilatation. All data were expressed as a percentage of maximal cutaneous vascular conductance (CVC) at each site (28 m m sodium nitroprusside; 43°C). Sodium excretion increased during the HS diet (P < 0.05). The plateau % CVCmax was reduced during HS (LS: 93 ± 1 % CVCmax vs. HS: 80 ± 2 % CVCmax; P < 0.05). During the HS diet, AA improved the plateau % CVCmax (Ringer: 80 ± 2 % CVCmax vs. AA: 89 ± 3 % CVCmax; P < 0.05) and restored the NO contribution (Ringer: 44 ± 3 % CVCmax vs. AA: 59 ± 6 % CVCmax; P < 0.05). These data demonstrate that dietary sodium loading impairs cutaneous microvascular function independent of BP in normotensive adults and suggest a role for oxidative stress.
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Reduced sodium diets improve endothelial function and nitric oxide bioavailability.
“We have previously demonstrated that reduced sodium diets result in improved endothelial function and nitric oxide bioavailability.13, 17, 21, 40”
From Reducing Dietary Sodium to 1000 mg per Day Reduces Neurovascular Transduction Without Stimulating Sympathetic Outflow (2019) · cites this paper as [40]
The Microvascular function results report better cutaneous vasodilation on the low-sodium than the high-sodium diet in normotensive adults with salt-resistant blood pressure. However, the difference in nitric oxide’s contribution between diets did not reach statistical significance (P = 0.075), and nitric oxide bioavailability was not directly measured. The claim therefore overstates that part of the finding and generalizes beyond the microvascular response studied. (LLM, conf=0.86)
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Voluntary Wheel Running Attenuates Salt-Induced Vascular Stiffness Independent of Blood Pressure
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Reducing Dietary Sodium Intake among Young Adults in Ghana: A Call to Action
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Self-citationEffects of Dietary Sodium Modulation on Circulating Extracellular Vesicles
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- Authors
- Greaney, J. L., DuPont, J. J., Lennon‐Edwards, S. L., Sanders, P. W., Edwards, D. G., & Farquhar, W. B.
- Affiliations
- University of Delaware (US)
- University of Alabama at Birmingham (US)
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2012-10-04
- Volume
- 590
- Issue
- 21
- Pages
- 5519-5528
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC3515835
- OpenAlex
- W2107741169
- Semantic Scholar
- ae7ae9eacce98c899313d615fad2d0b65a735415
- Cited by
- 119
- References
- 56
- Citations by year
- 2026: 3 · 2025: 10 · 2024: 6 · 2023: 11 · 2022: 10 · 2021: 8 · 2020: 17 · 2019: 16 · 2018: 8 · 2017: 5 · 2016: 7 · 2015: 5 · 2014: 7 · 2013: 3 · 2012: 3
- FWCI
- 5.38
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Physiology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Department of Veterans Affairs (P30 DK079337)
- National Institutes of Health (GM103446, DK079337)
- National Heart, Lung, and Blood Institute (R01HL104106)
- National Institute of General Medical Sciences (P20GM103446)
- 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
- high-salt diet, sodium restriction, microvascular function, cutaneous vascular conductance, oxidative stress, salt tolerance, normotensive subjects, vitamin C, antioxidant supplementation, nitric oxide-dependent vasodilation, sodium excretion, blood pressure, sodium reduction, L-NAME, sodium nitroprusside, microdialysis
- MeSH terms
- Adult, Antioxidants, Ascorbic Acid, Blood Pressure, Female, Humans, Male, Sodium, Dietary, Oxidative Stress, Microvessels
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