A novel mechanism for buffering dietary salt in humans: Effects of salt loading on skin sodium, VEGF-C and blood pressure
Wolters Kluwer Health
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Selvarajah, V., Mäki-Petäjä, K., Pedro, L., Bruggraber, S., Burling, K., Goodhart, A., Brown, M., et al. (2017). A novel mechanism for buffering dietary salt in humans: Effects of salt loading on skin sodium, VEGF-C and blood pressure. Hypertension, 70 (5), 930-937. https://doi.org/10.1161/HYPERTENSIONAHA.117.10003
High dietary sodium intake triggers increased blood pressure (BP). Animal studies show that dietary salt loading results in dermal Na+ accumulation and lymphangiogenesis mediated by VEGF-C (vascular endothelial growth factor C), both attenuating the rise in BP. Our objective was to determine whether these mechanisms function in humans. We assessed skin electrolytes, BP, and plasma VEGF-C in 48 healthy participants randomized to placebo (70 mmol sodium/d) and slow sodium (200 mmol/d) for 7 days. Skin Na+ and K+ concentrations were measured in mg/g of wet tissue and expressed as the ratio Na+:K+ to correct for variability in sample hydration. Skin Na+:K+ increased between placebo and slow sodium phases (2.91±0.08 versus 3.12±0.09; P=0.01). In post hoc analysis, there was a suggestion of a sex-specific effect, with a significant increase in skin Na+:K+ in men (2.59±0.09 versus 2.88±0.12; P=0.008) but not women (3.23±0.10 versus 3.36±0.12; P=0.31). Women showed a significant increase in 24-hour mean BP with salt loading (93±1 versus 91±1 mm Hg; P<0.001) while men did not (96±2 versus 96±2 mm Hg; P=0.91). Skin Na+:K+ correlated with BP, stroke volume, and peripheral vascular resistance in men but not in women. No change was noted in plasma VEGF-C. These findings suggest that the skin may buffer dietary Na+, reducing the hemodynamic consequences of increased salt, and this may be influenced by sex.
blood pressure, skin, sodium, stroke volume, vascular endothelial growth factor C
V. Selvarajah was funded by the British Heart Foundation (grant number FS/12/33/29561) and NIHR. I.B. Wilkinson is funded by the British Heart Foundation. I.B. Wilkinson, C.M. McEniery, and K.M. Mäki-Petäjä receive Cambridge NIHR Biomedical Research Centre–Comprehensive Clinical Research Network support. The Human Research Tissue Bank is supported by the NIHR Cambridge Biomedical Research Centre. We thank the Medical Research Council (grant number MC_US_A090_0008/Unit Programme number U1059) for their support.
British Heart Foundation (FS/12/33/29561)
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External DOI: https://doi.org/10.1161/HYPERTENSIONAHA.117.10003
This record's URL: https://www.repository.cam.ac.uk/handle/1810/267853
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