Abstract

Introduction: Dietary sodium is an important trigger for hypertension. Animal studies show that the skin buffers dietary salt and salt-loading induces lymphangiogenesis mediated by VEGF-C, maintaining normal BP. Our primary objective was to determine whether increased skin Na + on salt loading attenuates the expected rise in blood pressure. Methods: We assessed skin and urine electrolytes, systemic haemodynamics, ambulatory BP and plasma VEGF-C in 48 healthy participants. Participants were placed on a low salt diet (70mmol sodium/day) and received placebo and slow sodium (200mmol daily for 7 days) in a randomised order. Skin Na + and K + concentrations were measured in mg/g tissue by inductively coupled plasma optical emission spectroscopy. Results were expressed as the ratio of Na + :K + to correct for variability in sample hydration. Plasma VEGF-C was analysed by ELISA. Results: Mean age was 30 ± 8 years (24 male). 24-hr urine Na + was higher following salt than placebo in males (221.9 ± 16.5 vs. 86.3 ± 10.3mmol, p < 0.001) and females (227.1 ± 19.9 vs. 60.0 ± 6.8mmol, p < 0.001). In males, skin Na + :K + was higher after salt loading (2.87 ± 0.12 vs. 2.59 ± 0.09 mg/g , p = 0.008), but not significantly different in females (3.36 ± 0.12 vs. 3.23 ± 0.10 mg/g, p = 0.49). Females showed a significant increase in 24-hr MAP with salt loading (88 ± 1 vs. 85 ± 1 mmHg, p=0.004) but not males (90 ± 2 vs. 90 ± 2 mm Hg, p = 0.91). In males only, skin Na + :K + correlated with supine MAP post-placebo (r = 0.52, p = 0.004) and post-salt (r = 0.51, p = 0.01). No significant change was noted in plasma VEGF-C. Conclusions: Salt loading causes an increase in BP in healthy females but not in males, whilst skin sodium rises in males. This indicates that the skin may buffer the haemodynamic consequences of increased salt intake in a gender-specific manner.

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