Hypoxia-Related Disruptions in Beat-by-Beat Blood Pressure Regulation: Mechanisms and Implications for Health and Disease

Hypoxia is a common feature of arterial hypertension that does not consistently elevate blood pressure (BP), but it triggers exaggerated increases in muscle sympathetic nerve activity (MSNA) and may disturb sympathetic transduction and baroreflex sensitivity in hypertensive individuals. Elevated resting MSNA, enhanced vascular sympathetic transduction, and impaired baroreflex sensitivity are associated with increased blood pressure variability (BPV), a marker of target organ damage independent of absolute BP levels. We hypothesized that hypoxia would lead to greater BPV in hypertensive individuals. Nine men (stage 1–2 untreated hypertensive [HT] and normotensive [NT]) were exposed to normoxia (21% O₂) and isocapnic hypoxia (IH, 10% O₂). During both conditions, oxygen saturation, beat-to-beat BP, MSNA, and end-tidal carbon dioxide (PetCO₂) were monitored, with PetCO₂ 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 via the sequence technique, and sympathetic baroreflex sensitivity (sBRS) via MSNA-DBP regression. IH induced comparable oxygen desaturation in both groups. Although BP and PetCO₂ remained unchanged, MSNA responses were greater in HT (NT: +8 ± 2 vs. HT: +12 ± 2 bursts·min⁻¹, P = 0.03). IH increased all indices of BPV and sympathetic transduction, and 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.