Project description: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.
Project description:The aim of this study was to estimate the effects of dietary salt reduction on blood pressure (BP) in Chinese adults and the effects of China-specific cooking salt-reduction strategies (the use of salt substitutes and salt-restriction spoons). The PubMed and China National Knowledge Infrastructure databases were searched for studies satisfying the search criteria. Outcomes extracted from each included study were 24-h urinary sodium excretion, salt (sodium chloride) intake, and BP before and after dietary salt lowering. A random-effects meta-analysis was performed, and results were evaluated for evidence of publication bias and heterogeneity. Because most studies aggregated results for hypertensive and normotensive participants, estimates were made for hypertensive participants only and for hypertensive and normotensive participants combined. Six salt-restriction experiment studies (3,153 participants), 4 cooking salt-restriction spoon studies (3,715 participants), and 4 cooking salt-substitute studies (1,730 participants) were analyzed. In salt-restriction experiment studies, the pooled estimate of mean change in 24-h urinary sodium excretion in hypertensive participants was -163.0 mmol/day (95% confidence interval [CI]: -233.5 to -92.5 mmol/day), which was associated with a mean reduction of -8.9 mm Hg (95% CI: -14.1 to -3.7 mm Hg) in systolic BP. Each 1.00-g dietary salt reduction in hypertensive participants was associated with a reduction of 0.94 mm Hg in systolic BP (95% CI: 0.69 to 1.03 mm Hg). These systolic BP reductions in hypertensive participants were 1.71 times greater compared with the mixed hypertensive and normotensive group. Salt-restriction spoon studies demonstrated a 1.46-g decrease in daily salt intake level. The effect of salt-substitute use on systolic BP control was substantial among the hypertensive participants (-4.2 mm Hg; 95% CI: -7.0 to -1.3 mm Hg), but the change did not reach statistical significance in hypertensive and normotensive participants combined (-2.31 mm Hg; 95% CI: -5.57 to 0.94 mm Hg). Salt restriction lowers mean BP in Chinese adults, with the strongest effect among hypertensive participants. Future studies of salt-restriction strategies should be report results stratified by hypertension status and adjust for medication use.
Project description:Uromodulin, also named Tamm Horsfall protein, have been associated with renal function and sodium homeostasis regulation. The authors sought to examine the effects of salt intake on plasma and urinary uromodulin levels and the association of its genetic variants with salt sensitivity in Chinese adults. Eighty patients from our natural population cohort were maintained sequentially either on a usual diet for 3 days, a low-salt diet (3.0 g) for 7 days, and a high-salt diet (18.0 g) for an additional 7 days. In addition, the authors studied 514 patients of the Baoji Salt-Sensitive Study, recruited from 124 families who received the same salt intake intervention, and investigated the association of genetic variations in uromodulin gene with salt sensitivity. Plasma uromodulin levels were significantly lower on a high-salt diet than on a baseline diet (28.3 ± 4.5 vs. 54.9 ± 8.8 ng/ml). Daily urinary excretions of uromodulin were significantly decreased on a high-salt diet than on a low-salt diet (28.7 ± 6.7 vs. 157.2 ± 21.7 ng/ml). SNPs rs7193058 and rs4997081 were associated with the diastolic blood pressure (DBP), mean arterial pressure (MAP) responses to the high-salt diet. In addition, several SNPs in the uromodulin gene were significantly associated with pulse pressure (PP) response to the low-salt intervention. This study shows that dietary salt intake affects plasma and urinary uromodulin levels and that uromodulin may play a role in the pathophysiological process of salt sensitivity in the Chinese populations.
Project description:It is classically thought that it is the amount of salt that is critical for driving acute blood pressure responses. However, recent studies suggest that blood pressure responses, at least acutely, may relate to changes in serum osmolality. Here, we test the hypothesis that acute blood pressure responses to salt can be altered by concomitant water loading. Ten healthy patients free of any disease and medication underwent 4 interventions each a week apart in which they took 300 mL of lentil soup with no salt (visit 1), lentil soup with 3 g salt (visit 2), or lentil soup with 3 g salt and 500 mL water (visit 3) or 750 mL water (visit 4). At each visit, hourly blood measurements and blood pressure measurements (baseline, 1st, 2nd, 3rd, and 4th hour) were performed and plasma osmolarity, sodium and copeptin levels were measured. Patients receiving the 3 g salt showed a 6 mOsm/L change in osmolality with a 2.5 mmol/L change in plasma sodium and 10 mm Hg rise in systolic blood pressure at 2 hours. When the same patients drank salty soup with water, the changes in plasma osmolarity, plasma sodium, and blood pressure were prevented. The ability to raise blood pressure acutely with salt appears dependent on changes in plasma osmolality rather than the amount of salt. Our findings suggest that concurrent intake of water must be considered when evaluating the role of salt in blood pressure.