High Dietary Sodium Reduces Low‐Flow‐Mediated Constriction in Salt‐Resistant Adults

Abstract

High dietary sodium has been shown to impair flow‐mediated dilation independent of blood pressure (BP). Low flow‐mediated (LFC) constriction has been proposed as a complementary measure of vascular function in humans. Therefore, the purpose of this study was to test the hypothesis that a high sodium diet would reduce brachial artery LFC in salt‐resistant adults. Additionally, we sought to determine if sex differences existed in the LFC response to high dietary sodium. Twenty healthy, normotensive adults (12 males, 28.8±1.8 yrs; 8 females, 29.8±2.2 yrs) participated in a controlled feeding study. Following a run‐in diet, participants completed 7 days of a low sodium (LS) diet (20mmol sodium/day) and 7 days of a high sodium (HS) diet (300mmol sodium/day) in random order. Diets were designed to be eucaloric and consistent in macronutrient distribution and potassium content. On the last day of the LS and HS diets, a 24‐hour urine was collected and 24‐hour ambulatory BP was assessed. Subjects were classified as salt‐resistant as defined by a change in 24‐hour ambulatory mean arterial pressure (MAP) of ≤5mmHg between the LS and HS diets. On day 7 of the LS and HS diet, LFC was assessed by ultrasound. LFC was calculated as the % change in brachial artery diameter following a 5‐minute distal cuff occlusion. By design, 24‐hour MAP was not different between LS and HS conditions (85±1 vs 84±1 mmHg, p>0.05) whereas urinary sodium excretion (34.8±6.0mmol/24hr vs 269.7±21.6 mmol/24hr, p<0.01) and serum sodium concentration (137.9±0.6mmol/L vs 140.2±0.3mmol/L, p<0.01) increased significantly on the HS diet. LFC was significantly attenuated on the HS diet compared to LS (2.2±0.3% vs 3.3±0.3%). LFC was reduced by HS in both men and women (men: LS 3.8±0.4% vs HS 2.6±0.4%; women: LS 2.6±0.5% vs HS 1.5±0.5%; p<0.05). These data demonstrate that high dietary sodium impairs LFC in salt‐resistant adults providing additional evidence for the adverse vascular effects of dietary sodium independent of BP.Support or Funding InformationResearch funded by NIH grant R01 HL104106