Hypoxia Disrupts Neurovascular Regulation of Blood Pressure in Normotensive and Untreated Hypertensive Men

Hypoxia is a common feature of arterial hypertension that does not consistently elevate blood pressure (BP), but triggers exaggerated increases in muscle sympathetic nerve activity (MSNA) and may disturb sympathetic transduction and baroreflex sensitivity in hypertensive individuals. Elevated resting MSNA, enhanced sympathetic transduction, and reduced baroreflex sensitivity are all associated with increased blood pressure variability (BPV), a marker of target organ damage independent of absolute BP levels. We hypothesized that hypoxia would elicit greater BPV in hypertensive individuals. Nine young-to-middle-aged men with untreated stage 1–2 hypertension (HT) and normotensive controls (NT) were exposed to normoxia (21%O ₂ ) and isocapnic hypoxia (IH, 10%O ₂ ). During both conditions, oxygen saturation, beat-to-beat BP, MSNA, and end-tidal CO ₂ (PetCO ₂ ) were continuously monitored, with PetCO ₂ clamped. BPV was quantified using standard deviation, coefficient of variation, and average real variability for systolic (SBP), diastolic (DBP), and mean BP (MBP). Sympathetic transduction was assessed using a time-domain signal averaging technique. Cardiac baroreflex sensitivity (cBRS) was evaluated using the sequence method, and sympathetic baroreflex sensitivity (sBRS) was calculated via MSNA–DBP regression. IH induced comparable oxygen desaturation in both groups (NT: −25.7 ± 3.3% vs. HT: −21.2 ± 4.0%, p > 0.05). Although BP and PetCO ₂ remained unchanged, MSNA responses were significantly greater in HT (NT: +8 ± 2 vs. HT: +12 ± 2 bursts/min, p = 0.03). IH increased all indices of BPV and sympathetic transduction, while both cBRS and sBRS were similarly impaired in the two groups. In conclusion, IH similarly exacerbates BPV and disrupts sympathetic transduction and baroreflex function in normotensive and untreated hypertensive men, despite greater MSNA reactivity in the hypertensive group.