Effect of acute hypoxia on the time course change in flow‐mediated dilation: effect of sympathetic nerve activity (708.4)

Endothelium‐dependent flow‐mediated dilation (FMD) is impaired during exposure to high altitude. Although the time course and mechanism(s) governing this impairment are undefined, hypoxic‐induced elevations in sympathetic outflow may attenuate FMD. We examined the hypothesis that acute exposure to normobaric hypoxia would lead to reductions in FMD that could be reversed via adrenergic blockade. In a placebo‐controlled crossover experiment, brachial FMD, arterial oxygen saturation, blood pressure and heart rate (HR) were assessed in 11 healthy participants (aged 32±7 y) in normobaric normoxia and following 60 min, 210 min and 330 min of normobaric hypoxia (FIO 2 =0.11). At 210 min, participants ingested an α 1 ‐adrenoreceptor blocker (Prazosin; 1 mg/20 kg body mass) or an identical placebo. Compared to normoxic baseline, FMD was reduced following 60 min, 210, and 330 min of hypoxia by 1.6 ± 0.2% (relative change 28%), 2.5 ± 0.1% and 2.8 ± 0.2% (36%), respectively (P蠄0.003). Following α 1 ‐blockade, FMD and HR at 330 min were 5 ± 2 beats∙min ‐1 and 1.8 ± 1.4% (35%) higher compared with the placebo trial (P蠄0.03). In summary, sustained reductions in FMD occur within 60 min of exposure to normobaric hypoxia and are largely mediated via the α 1 ‐adrenoceptor pathway.