ADA and pulmonary arterial hypertension: Adenosine levels in the pulmonary circulation are pathologically low in patients with WHO group 1 pulmonary arterial hypertension (PAH) as a consequence of local endothelial dysfunction and increased inactivation by ADA, possibly indicating that adenosine A1AR and A2AAR activation deficits unbalanced by inosine-mediated A3AR tone (Herman-de-Sousa et al., 2020) may contribute to maladaptive lung disease (Saadjian et al., 1999).