At the cellular level, AMPK-α1/α2 deficiency was also associated with reduced KV1.5 channel availability but not expression in acutely isolated pulmonary arterial myocytes, which has also been indicated in animal models of PPHN52,53; representing perhaps another differentiating factor when compared to pulmonary hypertension secondary to congenital heart disease78. This evidence concerns the gene PRKAA1 and pulmonary arterial hypertension.