TY - JOUR
T1 - Short-term water deprivation does not increase blood pressure variability or impair neurovascular function in healthy young adults
AU - Watso, Joseph C.
AU - Robinson, Austin T.
AU - Babcock, Matthew C.
AU - Migdal, Kamila U.
AU - Wenner, Megan M.
AU - Stocker, Sean D.
AU - Farquhar, William B.
N1 - Funding Information:
This research was supported by the National Heart, Lung, and Blood Institute (R01-HL-128388; W. B. Farquhar and S. D. Stocker), the American Heart Association (18POST34060020; A. T. Robinson), and a University of Delaware Doctoral Fellowship (J. C. Watso). This publication was made possible by the Delaware COBRE program, supported by a grant from the National Institute of General Medical Sciences (5-P30-GM-113125) from the National Institutes of Health.
Publisher Copyright:
© 2020 the American Physiological Society
PY - 2020/1
Y1 - 2020/1
N2 - High dietary salt increases arterial blood pressure variability (BPV) in salt-resistant, normotensive rodents and is thought to result from elevated plasma [Na+] sensitizing central sympathetic networks. Our purpose was to test the hypothesis that water deprivation (WD)-induced elevations in serum [Na] augment BPV via changes in baroreflex function and sympathetic vascular transduction in humans. In a randomized crossover fashion, 35 adults [17 female/18 male, age: 25 + 4 yr, systolic/diastolic blood pressure (BP): 107 + 11/60 + 7 mmHg, body mass index: 23 + 3 kg/m2] completed two hydration protocols: a euhydration control condition (CON) and a stepwise reduction in water intake over 3 days, concluding with 16 h of WD. We assessed blood and urine electrolyte concentrations and osmolality, resting muscle sympathetic nerve activity (MSNA; peroneal microneurography; 18 paired recordings), beat-to-beat BP (photoplethysmography), common femoral artery blood flow (Doppler ultrasound), and heart rate (single-lead ECG). A subset of participants (n = 25) underwent ambulatory BP monitoring during day 3 of each protocol. We calculated average real variability as an index of BPV. WD increased serum [Na+] (141.0 + 2.3 vs. 142.1 + 1.7 mmol/L, P < 0.01) and plasma osmolality (288 + 4 vs. 292 + 5 mosmol/kg H2O, P < 0.01). However, WD did not increase beat-to-beat (1.9 + 0.4 vs. 1.8 + 0.4 mmHg, P = 0.24) or ambulatory daytime (9.6 + 2.1 vs. 9.4 + 3.3 mmHg, P = 0.76) systolic BPV. Additionally, sympathetic baroreflex sensitivity (P = 0.20) and sympathetic vascular transduction were not different after WD (P = 0.17 for peak mean BP following spontaneous MSNA bursts). These findings suggest that, despite modestly increasing serum [Na+], WD does not affect BPV, arterial baroreflex function, or sympathetic vascular transduction in healthy young adults.
AB - High dietary salt increases arterial blood pressure variability (BPV) in salt-resistant, normotensive rodents and is thought to result from elevated plasma [Na+] sensitizing central sympathetic networks. Our purpose was to test the hypothesis that water deprivation (WD)-induced elevations in serum [Na] augment BPV via changes in baroreflex function and sympathetic vascular transduction in humans. In a randomized crossover fashion, 35 adults [17 female/18 male, age: 25 + 4 yr, systolic/diastolic blood pressure (BP): 107 + 11/60 + 7 mmHg, body mass index: 23 + 3 kg/m2] completed two hydration protocols: a euhydration control condition (CON) and a stepwise reduction in water intake over 3 days, concluding with 16 h of WD. We assessed blood and urine electrolyte concentrations and osmolality, resting muscle sympathetic nerve activity (MSNA; peroneal microneurography; 18 paired recordings), beat-to-beat BP (photoplethysmography), common femoral artery blood flow (Doppler ultrasound), and heart rate (single-lead ECG). A subset of participants (n = 25) underwent ambulatory BP monitoring during day 3 of each protocol. We calculated average real variability as an index of BPV. WD increased serum [Na+] (141.0 + 2.3 vs. 142.1 + 1.7 mmol/L, P < 0.01) and plasma osmolality (288 + 4 vs. 292 + 5 mosmol/kg H2O, P < 0.01). However, WD did not increase beat-to-beat (1.9 + 0.4 vs. 1.8 + 0.4 mmHg, P = 0.24) or ambulatory daytime (9.6 + 2.1 vs. 9.4 + 3.3 mmHg, P = 0.76) systolic BPV. Additionally, sympathetic baroreflex sensitivity (P = 0.20) and sympathetic vascular transduction were not different after WD (P = 0.17 for peak mean BP following spontaneous MSNA bursts). These findings suggest that, despite modestly increasing serum [Na+], WD does not affect BPV, arterial baroreflex function, or sympathetic vascular transduction in healthy young adults.
KW - Arterial baroreflex function
KW - Blood pressure variability
KW - Hypohydration
KW - Serum sodium concentrations
KW - Sympathetic vascular transduction
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U2 - 10.1152/AJPREGU.00149.2019
DO - 10.1152/AJPREGU.00149.2019
M3 - Article
C2 - 31617739
AN - SCOPUS:85077404338
SN - 0363-6119
VL - 318
SP - R112-R121
JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology
IS - 1
ER -