We next investigated the impact of AMPK-α1/α2 deletion on voltage-gated potassium (KV) currents in acutely isolated pulmonary arterial smooth muscle cells, because reduced activity and/or expression of KV1.5 has been identified as a hallmark of persistent pulmonary hypertension in neonates52,53 and pulmonary hypertension in adults54,55, where it has been proposed to decrease K+ efflux and thus oppose apoptosis55–58. This evidence concerns the gene KCNA5 and pulmonary hypertension.