Short-term water deprivation does not increase blood pressure variability or impair neurovascular function in healthy young adults

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/m(2)] 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 Delta 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.