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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).

Original publication




Journal article


Jacc basic transl sci

Publication Date





176 - 186


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