Abstract
Current evidence suggests that the persistent sympathetic nerve activity (SNA), commonly observed following exposure to hypoxia (HX), is mediated by chemoreceptor sensitization and baroreflex resetting. Evidence in animals suggests that these reflexes may independently regulate the frequency (gating) and amplitude (neuronal recruitment) of SNA bursts. In humans (n=7) we examined the regulation of SNA following acute isocapnic HX (5 min; end‐tidal PO2 = 45 Torr) and euoxic hypercapnia (HC; 5 min; end‐tidal PCO2 = +10 from baseline). HX increased SNA burst frequency (21±7 to 28±8 Burst/min, P<0.05) and amplitude (99±10 to 125±19 au, P<0.05) as did HC (14±6 to 22±10 bursts/min, P<0.05 and 100±12 to 133±29 au, P<0.05 respectively). Burst frequency (26±7 bursts/min, P<0.05), but not amplitude (97±12 au), remained elevated 10 min post HX. Both frequency and amplitude decreased during recovery following HC. These data clearly indicate two separate mechanisms, related to HX, regulating the pattern and magnitude of sympathetic outflow in humans. This study was supported by NSERC.
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