Apelin agonism causes systemic vasodilatation and increased cardiac contractility in humans, and improves pulmonary arterial hypertension (PAH) in animal models. Here, the authors examined the short-term pulmonary hemodynamic effects of systemic apelin infusion in patients with PAH. In a double-blind randomized crossover study, 19 patients with PAH received intravenous (Pyr1)apelin-13 and matched saline placebo during invasive right heart catheterization. (Pyr1)apelin-13 infusion caused a reduction in pulmonary vascular resistance and increased cardiac output. This effect was accentuated in the subgroup of patients receiving concomitant phosphodiesterase type 5 inhibition. Apelin agonism is a novel potential therapeutic target for PAH. (Effects of Apelin on the Lung Circulation in Pulmonary Hypertension; NCT01457170).
Keywords: APJ; CO, cardiac output; FA, formic acid; NO, nitric oxide; PAEC, pulmonary artery endothelial cells; PAH, pulmonary arterial hypertension; PDE5, phosphodiesterase-5; PVR, pulmonary vascular resistance; SVR, systemic vascular resistance; apelin; human; pulmonary arterial hypertension.