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 (PETCO2) 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% CO2, 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: Delta 1.6 +/- 1.2 mmol/L vs. LSM: Delta 0.7 +/- 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.