Nitric oxide (NO) is critical in the regulation of vascular function. Vascular NO quantification is complex due to its short half-life and high reactivity. Exhaled NO has been being extensively as a surrogate measure of vascular NO bioavailability due to its ease of measurement. We have previously shown a lack of relationship between changes in exhaled and venous nitrite (NO2-) before and after an acute exercise challenge in normoxia (Evans & Bailey, 2011). We therefore wanted to extend this work by examining the relationship between exhaled NO and venous NO2- after a passive hypoxic exposure, since hypoxia can stimulate the generation of vascular NO. Exhaled NO and venous NO2- was quantified in sixteen apparently healthy males in normoxia and following a 6hr passive exposure hypoxia to (12% O2). Venous blood was collected from an indwelling catheter placed in an antecubital vein and was immediately centrifuged (2500rpm; 4oC). Plasma was flash frozen and stored at -80oC before later analysis. Both exhaled NO and plasma NO2- concentrations were measured using established ozone-chemiluminescence techniques (Sievers NOA 280i). Passive hypoxia elicited no change in either exhaled NO (Norm: 10 ± 7 vs. Hyp: 10 ± 8 ppb P > 0.05) or plasma NO2- (Norm: 201 ± 87 vs. Hyp: 209 ± 105nmol; P > 0.05) (Paired sample T-test). No relationship was observed between delta changes (hypoxia minus normoxia) in exhaled NO and plasma NO2- (r = 0.167, P>0.05) (Pearson’s correlation). Current data suggests there is no relationship between changes in exhaled NO and NO2-. This could be due to the fact that there were not any observable differences between absolute exhaled NO and NO2- concentrations. The use of exhaled NO should still therefore be used with caution when evaluating NO bioavailability and its physiological action. Exhaled NO could still over or under estimate vascular NO bioavailability.