Controversy rages as to the role of mitochondria-derived reactive oxygen species (ROS) in hypoxic pulmonary vasoconstriction (HPV). As a basic premise, exogenous ROS should mimic hypoxia if an elevation in ROS underlies HPV. Although peroxide does constrict pulmonary artery, this has only been shown for non-physiological levels. Thus, we examined the effects of low concentrations of peroxide on rat small PA. 10–100mM peroxide caused vasoconstriction, with a large transient and small sustained component. At 30mM peroxide the transient was 10 ± 3% of 80mM KCl induced tension (KPSS), and the sustained constriction 4 ± 1% (n=11). Constriction to peroxide was not inhibited by diltiazem or 2-APB (n=7). But it was significantly suppressed by genestein and Ro-318220 (p<0.05, n=7). HPV is potentiated by pretone, thus we examined this for peroxide. Pretone (~15% KPSS) induced by 27mM [K+] significantly potentiated peroxide-induced transient constrictions (to 51 ± 7% KPSS, n=7, p<0.001). Constriction induced by ROS thus shows some similarities to HPV. Whilst only providing circumstantial evidence that a rise in ROS might underlie HPV, these results predicate against the concept of a fall in ROS generation being the primary initiator of HPV. Funded by the British Heart Foundation.