INTERMITTENT HYPOXIA RELATED GENERATION OF REACTIVE OXYGEN SPECIES AND BAROREFLEX REGULATION OF BLOOD PRESSURE
Purpose: The intermittent hypoxia related generation of reactive oxygen species (ROS) associated with obstructive sleep apnea (OSA) increases sympathetic activity. However, the specific role of ROS in establishing the hypertension associated with chronic OSA has not been identified. We hypothesize that the intermittent hypoxia (IH) induced production of ROS will reset the operating point of the Carotid Baroreflex to a higher mean arterial pressure (MAP). Methods: Human subjects (n = 11, 5 female) underwent neck pressure/suction (NP/NS) to assess carotid baroreflex (CBR) function before and after intermittent hypoxia training with or without the antioxidant, N-acetyl cysteine (NAC). During NP/NS, mean arterial pressure was recorded non-invasively using a finometer. Following baseline measurements for hemodynamic variables and CBR function, subjects were asked to ingest a drink containing either NAC or a placebo. One hour after ingestion, hemodynamic variables and CBR function were again measured, following which the subjects were intermittent hypoxia trained (IHT). Immediately after IHT, hemodynamic and CBR function measurements were repeated three times 30 minutes apart. A two-way analysis of variance (ANOVA) was used to analyze differences between treatment groups across time. Results: There were no changes in CBR function with NAC versus placebo across time (p=0.791). In addition, the assessment of the operating point of the MAP with NAC versus placebo across time was not different (p=0.62). Conclusions: These data indicate that the known scavenging effect of ROS on central Nitric Oxide enabling a greater central sympathetic outflow was counteracted by an unidentified local vasodilation resulting in an unchanged MAP. The lack of increase in resting MAP following IHT is in agreement with previous studies that report no change in MAP after IHT.