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We thank Dr Chun and colleagues for their interest in our recent work, in which we show that homozygous deletion of the Erg or Aplnr gene results in pulmonary veno-occlusive disease in mice.1 In our article, we cited 3 studies demonstrating that Aplnr signaling had direct effects on venous circulation, and we stand by this statement. In the first study, entitled “Venous dilator effect of apelin, an endogenous peptide ligand for the orphan APJ receptor, in conscious rats,” Cheng and colleagues2 showed that in rats, pretreated with mecamylamine to cause ganglionic blockade followed by noradrenaline to restore venomotor tone, apelin caused a dose-dependent decrease in mean circulatory filling pressure despite greater reduction in mean arterial pressure, with the authors concluding that “apelin has a …

Response to Letter Regarding Article, “The ERG–APLNR Axis Controls Pulmonary Venule Endothelial Proliferation in Pulmonary Veno-Occlusive Disease”