Low-sodium DASH reduces oxidative stress and improves vascular function in salt-sensitive humans
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Salt induces oxidative stress in salt-sensitive (SS) animals and man. It is not known whether in SS subjects the low-sodium dietary approaches to stop hypertension (LS-DASH) reduces oxidative stress more than DASH, which is high in antioxidants. To assess the effects of DASH and LS-DASH on oxidative stress, 19 volunteers were studied after 3 weeks of a standardized usual low fruits and vegetables diet (ULFV), followed by 3 weeks on DASH (both diets approximately 120 mmol Na(+) per day), then 3 weeks on LS-DASH (60 mmol Na(+) per day). SS was defined as systolic blood pressure >or=5 mm Hg lower on LS-DASH than DASH. In SS subjects (N=9), systolic blood pressure was lower on LS-DASH (111.0+/-2.0 mm Hg) than DASH (118.0+/-2.2, P<0.01) and ULFV (122.3+/-2.7, P=0.002). In salt-resistant (SR) volunteers (N=10), systolic blood pressure was lower on DASH (113.0+/-1.6) than ULFV (119.0+/-1.8, P<0.05) but not LS-DASH (115.7+/-1.8). Urine F2-isoprostanes, a marker of oxidative stress, were lower in SS subjects on LS-DASH (1.69+/-0.24) than ULFV (3.09+/-0.50, P<0.05) and marginally lower than DASH (2.46+/-0.44, P<0.20). F2-isoprostanes were not different among the three diets in SR volunteers (2.18+/-0.29, 2.06+/-0.29, 2.27+/-0.53, respectively). Aortic augmentation index, a measure of vascular stiffness, was lower in SS subjects on LS-DASH than either DASH or ULFV, and lower on DASH than ULFV in SR volunteers. In SS but not SR subjects, LS-DASH is associated with lower values for F2-isoprostanes and the aortic augmentation index. The results suggest that LS-DASH decreases oxidative stress, improves vascular function and lowers blood pressure in SS but not SR volunteers.
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The spontaneously hypertensive stroke-prone rat (SHRSP), the most relevant experimental model of sporadic SVD, has multiple modest endothelial and perivascular tissue defects in early life, including impaired endothelial tight junctions, poor myelination, overactive microglia, and a tendency to glial scarring detectable in protein expression.
“the most relevant experimental model of sporadic SVD, the spontaneously-hypertensive stroke prone rat (SHRSP),21,22,135 has multiple modest endothelial and perivascular tissue defects in early life,21 including impaired endothelial tight junctions, poor myelination, overactive microglia, and tendency to glial scarring detectable in protein expression.134”
From Mechanisms of sporadic cerebral small vessel disease: insights from neuroimaging (2013) · cites this paper as [134]
In an animal model of spontaneous SVD, even modest short-term salt exposure exacerbated inflammation, oxidative stress and small vessel pathology, and to a lesser but measurable extent in control rats without raising blood pressure.
“In an animal model of spontaneous SVD, even modest short term salt exposure exacerbated inflammation, oxidative stress and small vessel pathology and to a lesser but nonetheless measureable extent in control rats without raising BP.134,135”
From Mechanisms of sporadic cerebral small vessel disease: insights from neuroimaging (2013) · cites this paper as [134]
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- Authors
- Al-Solaiman, Y., Jesri, A., Zhao, Y., Morrow, J. D., & Egan, B. M.
- Affiliations
- Medical University of South Carolina (US)
- Vanderbilt University (US)
- Corresponding author
- Egan, B M
- Venue
- Journal of Human Hypertension
- Published
- 2009-04-30
- Volume
- 23
- Issue
- 12
- Pages
- 826-835
- ISSN
- 0950-9240 (ISSN-L)
- 1476-5527
- PMC
- PMC2783838
- OpenAlex
- W2009794559
- Cited by
- 102
- References
- 64
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 4 · 2023: 4 · 2022: 4 · 2021: 6 · 2020: 7 · 2019: 5 · 2018: 7 · 2017: 5 · 2016: 7 · 2015: 10 · 2014: 12 · 2013: 11 · 2012: 6
- FWCI
- 5.16
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Human Hypertension (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Medical University of South Carolina
- National Institutes of Health
- National Heart, Lung, and Blood Institute (HL04290, K24HL004290, R01HL058794, HL 58794)
- National Institute of General Medical Sciences (GM 15431, P50GM015431, P01GM015431)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK 48831, R01DK048831)
- National Center on Minority Health and Health Disparities
- National Center for Research Resources (M01RR001070, RR-01070)
- National Institute on Minority Health and Health Disparities (P60MD000267, MD00267)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Sodium Intake and Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- salt-sensitive hypertension, oxidative stress, F2-isoprostanes, vascular function, aortic augmentation index, vascular stiffness, systolic blood pressure, dietary sodium reduction, antioxidants, hypertension prevention, dietary intervention, blood pressure reduction
- MeSH terms
- Adult, Aldosterone, Aorta, Blood Pressure, Cardiac Output, Diet, Sodium-Restricted, Elasticity, Electrolytes, Female, Heart Rate, Humans, Hypertension, Insulin, Lipids, Male, Middle Aged, Phenols, Plant Extracts, Potassium Chloride, Renin, Sodium Chloride, Vascular Resistance, Oxidative Stress, F2-Isoprostanes, Young Adult
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