A high salt meal does not impair cerebrovascular reactivity in healthy young adults

A high sodium (Na(+)) meal impairs peripheral vascular function. In rodents, chronic high dietary Na(+) impairs cerebral vascular function, and in humans, habitual high dietary Na(+) is associated with increased stroke risk. However, the effects of acute high dietary Na(+) on the cerebral vasculature in humans are unknown. The purpose of this study was to determine if acute high dietary Na(+) impairs cerebrovascular reactivity in healthy adults. Thirty‐seven participants (20F/17M; 25 ± 5 years; blood pressure [BP]: 107 ± 9/61 ± 6 mm Hg) participated in this randomized, cross‐over study. Participants were given a low Na(+) meal (LSM; 138 mg Na(+)) and a high Na(+) meal (HSM; 1,495 mg Na(+)) separated by ≥ one week. Serum Na(+), beat‐to‐beat BP, middle cerebral artery velocity (transcranial Doppler), and end‐tidal carbon dioxide (P(ET)CO(2)) were measured pre‐ (baseline) and 60 min post‐prandial. Cerebrovascular reactivity was assessed by determining the percent change in middle cerebral artery velocity to hypercapnia (via 8% CO(2), 21% oxygen, balance nitrogen) and hypocapnia (via mild hyperventilation). Peripheral vascular function was measured using brachial artery flow‐mediated dilation (FMD). Changes in serum Na(+) were greater following the HSM (HSM: Δ1.6 ± 1.2 mmol/L vs. LSM: Δ0.7 ± 1.2 mmol/L, p < .01). Cerebrovascular reactivity to hypercapnia (meal effect: p = .41) and to hypocapnia (meal effect: p = .65) were not affected by the HSM. Contrary with previous findings, FMD was not reduced following the HSM (meal effect: p = .74). These data suggest that a single high Na(+) meal does not acutely impair cerebrovascular reactivity, and suggests that despite prior findings, a single high Na(+) meal does not impair peripheral vascular function in healthy adults.