Journal article
Relaxin treatment reduces angiotensin II-induced vasoconstriction in pregnancy and protects against endothelial dysfunction
SA Marshall, CH Leo, JE Girling, M Tare, S Beard, NJ Hannan, LJ Parry
Biology of Reproduction | OXFORD UNIV PRESS INC | Published : 2017
Abstract
The peptide relaxin has gained considerable attention as a new vasoactive drug, largely through its beneficial therapeutic effects in cardiovascular disease. In this study, we tested the hypothesis that relaxin treatment alleviates systemic vascular dysfunction characteristic of hypertensive diseases of pregnancy. We investigated vascular effects and mechanisms of relaxin action in (i) pregnant relaxin-deficient (Rln-/-) mice with enhanced responses to angiotensin II (AngII) and (ii) arteries pre-incubated ex vivo in trophoblast conditioned media (TCM) to induce endothelial dysfunction. Pregnant Rln-/- mice received 0.5 μg/h recombinant human H2 relaxin (rhRLX: n = 5) or placebo (20 nM sodiu..
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Funding Acknowledgements
This work was supported by Australian National Health & Medical Research Council Project Grants (LJP, NH, MT), an Australian Research Council Linkage Grant (LJP, MT), and a University of Melbourne Research Scholarship and the David Lachlan Hay Postgraduate Writing Up-Award (SAM). NJH received salary support from The University of Melbourne (CR Roper Fellowship). This project was partially funded by Novartis Pharma AG, who provided the relaxin as a condition of an Australian Research Council Linkage Grant. LJP was also a paid consultant for Novartis Pharma AG. Novartis Pharma AG had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.