Strikingly, induction of hypoxic pulmonary vasoconstriction (HPV) and thus acute hypoxic pulmonary hypertension by mild hypoxia (8% O2) was virtually abolished in all AMPK-α1/α2 knockouts, SPV declining by only −77 ± 7 mm/s (n = 4) during 2 min exposures to 8% O2, compared to a net fall of −246 ± 27 mm/s for controls (n = 7, P = 0.006; Fig. 6aiv and Supplementary Fig. 10b). This evidence concerns the gene PRKAA1 and pulmonary arterial hypertension.