Selvarajah Viknesh, Mäki-Petäjä Kaisa M, Pedro Liliana, Bruggraber Sylvaine F A, Burling Keith, Goodhart Anna K, Brown Morris J, McEniery Carmel M, Wilkinson Ian B
From the Division of Experimental Medicine and Immunotherapeutics, University of Cambridge, United Kingdom (V.S., K.M.M-P., A.K.G., C.M.M., I.B.W.); MRC Human Nutrition Unit, Cambridge, United Kingdom (L.P., S.F.A.B.); NIHR Cambridge Biomedical Research Centre, Core Biochemical Assay Laboratory, United Kingdom (K.B.); and William Harvey Research Institute, Queen Mary University of London, United Kingdom (M.J.B.).
Hypertension. 2017 Nov;70(5):930-937. doi: 10.1161/HYPERTENSIONAHA.117.10003. Epub 2017 Oct 3.
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; =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; =0.008) but not women (3.23±0.10 versus 3.36±0.12; =0.31). Women showed a significant increase in 24-hour mean BP with salt loading (93±1 versus 91±1 mm Hg; <0.001) while men did not (96±2 versus 96±2 mm Hg; =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.
高膳食钠摄入量会引发血压升高。动物研究表明，膳食盐负荷会导致皮肤钠蓄积以及由血管内皮生长因子C（VEGF-C）介导的淋巴管生成，二者均可减轻血压升高。我们的目的是确定这些机制在人类中是否起作用。我们对48名健康参与者进行了评估，这些参与者被随机分为安慰剂组（70 mmol钠/天）和缓释钠组（200 mmol/天），为期7天。测量皮肤中钠和钾的浓度，以毫克/克湿组织表示，并以钠钾比来校正样本水化的变异性。安慰剂组和缓释钠组之间皮肤钠钾比升高（2.91±0.08对3.12±0.09；P=0.01）。在事后分析中，提示存在性别特异性效应，男性皮肤钠钾比显著升高（2.59±0.09对2.88±0.12；P=0.008），而女性则无变化（3.23±0.10对3.36±0.12；P=0.31）。盐负荷后，女性24小时平均血压显著升高（93±1对91±1 mmHg；P<0.001），而男性则无变化（96±2对96±2 mmHg；P=0.91）。男性中皮肤钠钾比与血压、每搏输出量和外周血管阻力相关，而女性中则无此相关性。血浆VEGF-C未发现变化。这些发现表明，皮肤可能缓冲膳食钠，减少盐摄入增加的血流动力学后果，且这可能受性别影响。
