Abstract
Relaxin is a peptide related to pregnancy that induces nitric oxide-related and gelatinase-related effects, allowing vasodilation and pregnancy-related adjustments permitting parturition to occur. Relaxin controls the hemodynamic and renovascular adaptive changes that occur during pregnancy. Interest has evolved regarding relaxin and a therapeutic principle in preeclampsia and heart failure. Preeclampsia is a pregnancy disorder, featuring hypertension, proteinuria and placental anomalies. We investigated relaxin in an established transgenic rat model of preeclampsia, where the phenotype is induced by angiotensin (Ang)-II production in mid pregnancy. We gave recombinant relaxin to preeclamtic rats at day 9 of gestation. Hypertension and proteinuria was not ameliorated after relaxin administration. Intrauterine growth retardation of the fetus was unaltered by relaxin. Heart-rate responses and relaxin levels documented drug effects. In this Ang-II-based model of preeclampsia, we could not show a salubrious effect on preeclampsia.
Highlights
Preeclampsia is one of the leading causes of maternal and fetal mortality and morbidity, complicating 3–8% of pregnancies.[1]
In pregnant rats naturally occurring rat relaxin serum levels were increased during pregnancy no differences in relaxin serum concentration between nontransgenic SpragueDawley (SD) rats and transgenic preeclamptic rats were observed (Fig 1A)
Relaxin did not ameliorate the preeclamptic phenotype in our transgenic rat model it showed biological activity
Summary
Preeclampsia is one of the leading causes of maternal and fetal mortality and morbidity, complicating 3–8% of pregnancies.[1] The disease is characterized by new onset of maternal hypertension after 20th week of gestation and proteinuria or in association with thrombocytopenia, impaired liver function, the new development of renal insufficiency, pulmonary edema, or new-onset of cerebral or visual disturbances.[2] Preeclampsia originates in the placenta, but the underlying etiology is complex and probably heterogeneous in origin.[1]. Impaired endovascular trophoblast invasion and vascular remodeling of the spiral artery is an early, but not necessarily the primary, pathology involved in preeclampsia.[3] The clinical syndrome “preeclampsia” might result from imbalance between factors produced by the placenta in response to abnormal placentation and maternal adaptation to them leading to PLOS ONE | DOI:10.1371/journal.pone.0150743. The clinical syndrome “preeclampsia” might result from imbalance between factors produced by the placenta in response to abnormal placentation and maternal adaptation to them leading to PLOS ONE | DOI:10.1371/journal.pone.0150743 March 10, 2016
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