High Sodium Intake Differentially Impacts Brachial Artery Flow Mediated Dilation When Evaluated with Reactive Versus Active Hyperemia

Abstract

OBJECTIVEThis study sought to determine if a high sodium (HS) intake attenuates upper limb flow mediated dilation in response to reactive (RH‐FMD) and sustained (SS‐FMD) hyperemia, and the role of oxidative stress in this response. Our hypothesis is HS intake will similarly impair upper limb vascular function when assessed as both RH‐FMD and SS‐FMD, and that this dysfunction will be reversed following acute antioxidant consumption.METHODSTen young, salt resistant participants (9 Males, 1 Female) consumed a 7‐day HS (6,900 mg/day) or a 7‐day low sodium (LS: 2,300 mg/day) diet in a randomized order. On the last day of the diet, brachial artery RH‐FMD (evaluated after 5 minutes of cuff occlusion) and SS‐FMD (handgrip exercise) were performed following consumption of placebo (PL) and repeated two hours after the consumption of antioxidants [AO; (1000 mg of vitamin C, 800 IU of vitamin E, and 400 mg of alpha lipoic acid]. Handgrip exercise (HG) was performed in 3‐minute workloads, increasing by 8 kg until failure, at a rate of one contraction per second. RH‐FMD responses were evaluated as percentage change from baseline and SS‐FMD was evaluated as brachial artery shear‐to‐dilation slopes assessed across all HG workloads achieved.RESULTSBetween diets, sodium consumption and excretion were significantly greater in the HS condition (p < 0.05 for both), but mean arterial blood pressure was unchanged (LS 85 ± 5; HS 84 ± 7 mmHg; p = 0.5). RH‐FMD was significantly lower during HS compared to LS (p = 0.01), in the placebo condition but not during the AO condition (p = 0.7), with a significant interaction present (HS+PL: 5.9 ± 3.4; HS+AO: 8.2 ± 2.7; LS+PL: 8.8 ± 4.7; LS+AO: 7.0 ± 2.1 %; p = 0.01) due to a significant increase in the HS+AO condition. A comparison of shear‐dilation slopes during SS‐FMD revealed no differences between sodium interventions (p = 0.3), AO condition (p = 0.1), or any interaction effect (p = 0.7) [HS+PL: 0.0031 ± 0.0013; HS+AO: 0.0026 ± 0.0012; LS+PL: 0.0028 ± 0.0012; LS+AO: 0.0022 ± 0.0010; mm.seconds‐1.kg‐1].CONCLUSIONIndependent of changes in MAP, a HS intake impaired peripheral vascular function when assessed via RH‐FMD, which was restored with AO consumption, potentially implicating elevated oxidative stress as a contributor to this dysfunction. However, SS‐FMD, evaluated via HG exercise, was not altered by a HS intake or AO consumption. In conclusion, 7‐days of a HS intake appears to have disparate effects between the two peripheral vascular function techniques, implicating an inability of HS intake to impact exercise‐induced BA dilation.