Abstract

Hypoxia may sensitize the carotid chemoreceptors resulting in a sustained elevation of muscle sympathetic nerve activity (MSNA) which outlasts the hypoxic stimulus. To test this hypothesis we determined (n=4) the effect of carotid body deactivation on the sustained elevation in MSNA (common peroneal nerve) following isocapnic hypoxia (arterial O2 saturation 80% for 20 mins) in humans. Ventilation, heart rate and MSNA were elevated in hypoxia; however, only the elevation in MSNA outlasted the hypoxic stimulus, and remained elevated for 20 mins following the hypoxic stimulus. In contrast, carotid body deactivation with hyperoxia (100% O2 for 1 min) transiently reduced MSNA in eight of nine trials (mean decrease 12.6 ± 9.5%, p = 0.005). Our results suggest that input from the carotid chemoreceptors is obligatory for the sustained elevation in MSNA initiated by chemoreflex stimulation. We attribute the decrease in MSNA to a transient hyperoxia‐induced attenuation in carotid chemoreceptor sensitivity.Research support: NSERC, MSFHR

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