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      Short-Term Hemodynamic Effects of Apelin in Patients With Pulmonary Arterial Hypertension

      research-article
      Author(s): , MD a , , MD c , , MD a , , MD a , , MD c , , MD c , , MBChB a , , MD a , , MBChB a , , PhD d , , MD a , , MD b , , MBChB a , , MD c , , MD c , , MS d , , PhD a , , MD b , , MD a , ∗
      Publication date (Electronic):
      Journal: Jacc. Basic to Translational Science
      Publisher: Elsevier on behalf of the American College of Cardiology Foundation
      Keywords: apelin, APJ, human, pulmonary arterial hypertension, 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

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          • •

            The effects of apelin on pulmonary hemodynamics in patients with PAH are unknown.

          • •

            Systemic infusion caused a significant reduction in pulmonary vascular resistance and increase in cardiac output without a change in heart rate or systemic vascular resistance.

          • •

            This effect was most prominent in the subgroup of patients receiving concomitant PDE5 inhibition.

          • •

            Apelin agonism is a novel potential therapeutic target for PAH.

          Summary

          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 (Pyr 1)apelin-13 and matched saline placebo during invasive right heart catheterization. (Pyr 1)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)

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          Most cited references16

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          Cellular and molecular basis of pulmonary arterial hypertension.

          Nicholas Morrell, Serge Adnot, Stephen Archer … (2009)
          Pulmonary arterial hypertension (PAH) is caused by functional and structural changes in the pulmonary vasculature, leading to increased pulmonary vascular resistance. The process of pulmonary vascular remodeling is accompanied by endothelial dysfunction, activation of fibroblasts and smooth muscle cells, crosstalk between cells within the vascular wall, and recruitment of circulating progenitor cells. Recent findings have reestablished the role of chronic vasoconstriction in the remodeling process. Although the pathology of PAH in the lung is well known, this article is concerned with the cellular and molecular processes involved. In particular, we focus on the role of the Rho family guanosine triphosphatases in endothelial function and vasoconstriction. The crosstalk between endothelium and vascular smooth muscle is explored in the context of mutations in the bone morphogenetic protein type II receptor, alterations in angiopoietin-1/TIE2 signaling, and the serotonin pathway. We also review the role of voltage-gated K(+) channels and transient receptor potential channels in the regulation of cytosolic [Ca(2+)] and [K(+)], vasoconstriction, proliferation, and cell survival. We highlight the importance of the extracellular matrix as an active regulator of cell behavior and phenotype and evaluate the contribution of the glycoprotein tenascin-c as a key mediator of smooth muscle cell growth and survival. Finally, we discuss the origins of a cell type critical to the process of pulmonary vascular remodeling, the myofibroblast, and review the evidence supporting a contribution for the involvement of endothelial-mesenchymal transition and recruitment of circulating mesenchymal progenitor cells.
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            The novel peptide apelin lowers blood pressure via a nitric oxide-dependent mechanism.

            Kazuhiko Tatemoto, Kiyoshige Takayama, Min-Xu Zou … (2001)
            Apelin is an endogenous ligand of the human orphan receptor APJ. We detected apelin-like immunoreactivity in the adipocytes, gastric mucosa, and Kupffer cells in the liver. We also detected apelin-like immunoreactivity localized within the endothelia of small arteries in various organs. Further, it was found that mean arterial pressure after the administration of apelin-12, apelin-13, and apelin-36 at a dose of 10 nmol/kg in anaesthetized rats was reduced by 26+/-5, 11+/-4, and 5+/-4 mm Hg, respectively. In the presence of a nitric oxide (NO) synthase inhibitor, the effect of apelin-12 on blood pressure was abolished. Furthermore, the administration of apelin-12 (10 nmol/kg) in rats produced a transitory elevation of the plasma nitrite/nitrate concentration from a basal level of 21.4+/-1.6 to 27.0+/-1.5 microM. Thus, apelin may lower blood pressure via a nitric oxide-dependent mechanism.
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              Treatment goals of pulmonary hypertension.

              Vallerie V McLaughlin, Luke S G E Howard, M Palazzini … (2013)
              With significant therapeutic advances in the field of pulmonary arterial hypertension, the need to identify clinically relevant treatment goals that correlate with long-term outcome has emerged as 1 of the most critical tasks. Current goals include achieving modified New York Heart Association functional class I or II, 6-min walk distance >380 m, normalization of right ventricular size and function on echocardiograph, a decreasing or normalization of B-type natriuretic peptide (BNP), and hemodynamics with right atrial pressure 2.5 mg/kg/min(2). However, to more effectively prognosticate in the current era of complex treatments, it is becoming clear that the "bar" needs to be set higher, with more robust and clearer delineations aimed at parameters that correlate with long-term outcome; namely, exercise capacity and right heart function. Specifically, tests that accurately and noninvasively determine right ventricular function, such as cardiac magnetic resonance imaging and BNP/N-terminal pro-B-type natriuretic peptide, are emerging as promising indicators to serve as baseline predictors and treatment targets. Furthermore, studies focusing on outcomes have shown that no single test can reliably serve as a long-term prognostic marker and that composite treatment goals are more predictive of long-term outcome. It has been proposed that treatment goals be revised to include the following: modified New York Heart Association functional class I or II, 6-min walk distance ≥ 380 to 440 m, cardiopulmonary exercise test-measured peak oxygen consumption >15 ml/min/kg and ventilatory equivalent for carbon dioxide 2.5 to 3.0 l/min/m(2). Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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                Author and article information

                Contributors
                Andrew J. Peacock
                Journal
                Journal ID (nlm-ta): JACC Basic Transl Sci
                Journal ID (iso-abbrev): JACC Basic Transl Sci
                Title: Jacc. Basic to Translational Science
                Publisher: Elsevier on behalf of the American College of Cardiology Foundation
                ISSN (Electronic): 2452-302X
                Publication date PMC-release: 28 March 2018
                Publication date Collection: April 2018
                Publication date (Electronic): 28 March 2018
                Volume: 3
                Issue: 2
                Pages: 176-186
                Affiliations
                [a ]Scottish Pulmonary Vascular Unit, Golden Jubilee National Hospital, Glasgow, United Kingdom
                [b ]British Heart Foundation/University of Edinburgh Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom
                [c ]National Pulmonary Hypertension Service–London, Department of Cardiac Sciences, Hammersmith Hospital, Imperial College Healthcare NHS Trust, London, United Kingdom
                [d ]Bristol-Myers Squibb Company, Discovery R&D, Princeton, New Jersey
                Author notes
                [∗ ] Address for correspondence: Prof. Andrew J. Peacock, Scottish Pulmonary Vascular Unit, Golden Jubilee National Hospital, Agamemnon Street, Glasgow G81 4DY, United Kingdom. apeacock@ 123456udcf.gla.ac.uk
                Article
                Publisher ID: S2452-302X(18)30056-1
                DOI: 10.1016/j.jacbts.2018.01.013
                PMC ID: 5981010
                PubMed ID: 29876530
                SO-VID: 18c16c61-6322-4743-a81a-0787c81c1cdc
                Copyright © © 2018 The Authors
                License:

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Date received : 23 October 2017
                Date revision received : 2 December 2017
                Date accepted : 13 January 2018
                Categories
                Subject: Article

                Keywords: apelin,apj,human,pulmonary arterial hypertension,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
                Data availability:
                Keywords: apelin, apj, human, pulmonary arterial hypertension, 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

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