High sodium intake differentially impacts brachial artery dilation when evaluated with reactive versus active hyperemia in salt resistant individuals.

This study sought to determine if high sodium (HS) intake in salt resistant (SR) individuals attenuates upper limb arterial dilation in response to reactive (occlusion) and active (exercise) hyperemia, two stimuli with varying vasodilatory mechanisms, and the role of oxidative stress in this response. Ten young, SR participants (9 males, 1 female) consumed a 7-day HS (6,900 mg/day) and a 7-day recommended sodium intake (RI: 2,300 mg/day) diet in a randomized order. On the last day of each diet, brachial artery (BA) function was evaluated via reactive (RH-FMD: 5 min of cuff occlusion) and active [handgrip (HG) exercise] hyperemia after consumption of both placebo (PL) and antioxidants (AO). The HS diet significantly elevated sodium excretion ( < 0.05), but mean arterial blood pressure was unchanged. During the PL condition, the HS diet significantly reduced RH-FMD when compared with RI diet ( = 0.01), but this reduction was significantly restored ( = 0.01) when supplemented with AO (HS + PL: 5.9 ± 3.4; HS + AO: 8.2 ± 2.7; RI + PL: 8.9 ± 4.7; RI + AO: 7.0 ± 2.1%). BA shear-to-dilation slopes, evaluated across all HG exercise workloads, were not significantly different across sodium intervention or AO supplementation. In SR individuals, HS intake impaired BA function when assessed via RH-FMD, but was restored with acute AO consumption suggesting oxidative stress as a contributor to this dysfunction. However, exercise-induced BA dilation was unaltered, potentially implicating an inability of HS intake to influence the mechanisms responsible for effectively maintaining skeletal muscle perfusion during exercise. This study examined if high sodium (HS) intake in salt resistant (SR) individuals attenuates brachial artery (BA) flow-mediated dilation in response to reactive (occlusion) and active (exercise) hyperemia. In SR individuals, HS intake impaired reactive hyperemia-induced BA dilation, but not exercise-induced BA dilation. This finding suggests that although brachial artery nitric oxide bioavailability may be reduced following HS intake, the redundant mechanisms associated with adequate upper limb blood flow regulation during exercise are maintained.