{"id":"a86419a917e6","type":"article","url":"https://hartvaat.nl/2017/11/01/zoutbuffering-in-de-huid-bij-mensen-een-nieuw-mechanisme/","title":"Zoutbuffering in de huid bij mensen: een nieuw mechanisme","title_en":"Novel Mechanism for Buffering Dietary Salt in Humans: Effects of Salt Loading on Skin Sodium, Vascular Endothelial Growth Factor C, and Blood Pressure.","category":"hypertensie","category_label":"Hypertensie","professions":["cardioloog","internist"],"tags":[],"journal":"Hypertension (Dallas, Tex. : 1979)","doi":"10.1161/HYPERTENSIONAHA.117.10003","source_url":"https://doi.org/10.1161/HYPERTENSIONAHA.117.10003","authors":["Viknesh Selvarajah","Kaisa M Mäki-Petäjä","Liliana Pedro","Sylvaine F A Bruggraber","Keith Burling","Anna K Goodhart","Morris J Brown","Carmel M McEniery","Ian B Wilkinson"],"significance":6,"published":"2017-11-01","source_date":"2017-11-01","image":"","kennis":["https://hartvaat.nl/kennis/hypertensie/hypertensie-en-ckd/"],"congress":"","summary_en":"This study described a novel mechanism for dietary salt buffering in human skin, showing that sodium is stored in skin tissue and triggers VEGF-C-mediated lymphangiogenesis, fundamentally changing the understanding of sodium homeostasis.","created":"2026-07-03T10:26:59Z","updated":"2026-07-03T13:26:15Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Studie die een nieuw mechanisme beschrijft voor zoutbuffering in de menselijke huid via natrium-opslag en VEGF-C. Verandert het begrip van zoutbalans en bloeddrukregulatie.","abstract_original":"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."}