(14-03-11) Endothelial function is impaired after a high-salt meal in healthy subjects1,2,3

1. Kacie M Dickinson,
2. Peter M Clifton, and
3. Jennifer B Keogh
+ Author Affiliations
1. 1From Preventative Health Flagship, Commonwealth Scientific and Industrial Research Organisation, Food and Nutritional Science, Adelaide, Australia (KMD, PMC, and JBK); the Discipline of Physiology, Faculty of Health Science, University of Adelaide, Adelaide, Australia (KMD, PMC, and JBK); the National Health and Medical Research Council of Australia Centre of Clinical Research Excellence in Nutritional Physiology, Interventions and Outcomes, Adelaide, Australia (KMD and PMC); Baker IDI, Heart & Diabetes Institute, Adelaide, Australia (PMC); and the Sansom Institute for Health Research, Division of Health Sciences, University of South Australia, Adelaide, Australia (JBK).
? ↵2 Supported by the Obesity & Health Theme, CSIRO Preventative Health Flagship.
? ↵3 Address correspondence to KM Dickinson, CSIRO Food & Nutritional Science, PO Box 10041 BC, Adelaide, South Australia 5000. E-mail: [email protected].
Abstract
Background: Dietary salt is related to blood pressure (BP), and cardiovascular disease and increased sodium intakes have been shown to impair vascular function. The effect of salt on endothelial function postprandially is unknown.
Objective: The aim was to investigate the postprandial effect of dietary salt on endothelial function as measured by flow-mediated dilatation (FMD) and peripheral arterial tonometry in healthy subjects.
Design: Sixteen healthy, normotensive subjects received a meal with added salt (HSM; 65 mmol Na) and a control low-salt meal (LSM; 5 mmol Na) on 2 separate occasions in a randomized order. Endothelial function was measured while fasting and postprandially at 30, 60, 90, and 120 min by using FMD and reactive hyperemia peripheral arterial tonometry. BP was also measured.
Results: Baseline FMD, reactive hyperemia index (RHI), and BP values were similar across interventions. Overall FMD was reduced 2 h postprandially. FMD was significantly more impaired after the HSM than after the LSM at 30 min [HSM (mean ? SD): 3.39 ? 2.44%; LSM: 6.05 ? 3.21%; P < 0.01] and at 60 min (HSM: 2.20 ? 2.77%; LSM: 4.64 ? 2.48%; P < 0.01). No significant differences in BP or RHI were observed between meals.
Conclusions: An HSM, which reflects the typical amount of salt consumed in a commonly eaten meal, can significantly suppress brachial artery FMD within 30 min. These results suggest that high salt intakes have acute adverse effects on vascular dilatation in the postprandial state. This trial was registered at www.anzctr.org.au/trial_view.aspx?ID=335115 as ACTRN12610000124033

Source: Am J Clin Nutr March 2011 vol. 93 no. 3 500-505

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