We aimed to confirm that a G protein biased compound produces vasodilatation in vivo, (the main mechanism of action for most current PAH therapies) without desensitization, as recent studies have suggested that apelin-mediated vasodilatation may occur via β-arrestin signaling (El Messari et al., 2004; Iturrioz et al., 2010; Ceraudo et al., 2014). Here, APLN is linked to pulmonary arterial hypertension.