TY - JOUR
T1 - A high salt meal does not impair cerebrovascular reactivity in healthy young adults
AU - Migdal, Kamila U.
AU - Robinson, Austin T.
AU - Watso, Joseph C.
AU - Babcock, Matthew C.
AU - Lennon, Shannon L.
AU - Martens, Christopher R.
AU - Serrador, Jorge M.
AU - Farquhar, William B.
N1 - Publisher Copyright:
© 2020 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society
PY - 2020/10/1
Y1 - 2020/10/1
N2 - 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: 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.
AB - 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: 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.
KW - cerebrovascular reactivity
KW - dietary sodium
KW - flow mediated dilation
KW - reactive oxygen species
KW - transcranial Doppler ultrasound
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U2 - 10.14814/phy2.14585
DO - 10.14814/phy2.14585
M3 - Article
C2 - 33038066
AN - SCOPUS:85092600007
SN - 2051-817X
VL - 8
JO - Physiological Reports
JF - Physiological Reports
IS - 19
M1 - e14585
ER -