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S Reini, Department of Physiology and Functional Genomics, University of Florida, Gainesville, United States
G Dutta, Department of Pharmacodynamics, University of Florida, gainesville, United States
C Wood, Department of Physiology and Functional Genomics, University of Florida, Gainesville, United States
M Keller-Wood, Department of Pharmacodynamics, University of Florida, Gainesville, United States

Correspondence: Maureen Keller-Wood, Email: kellerwd{at}cop.ufl.edu

Abstract

Previous studies have demonstrated that modest, physiologically relevant increases in maternal cortisol in late gestation result in enlargement of the fetal heart. In this study, we investigated the role of mineralocorticoid (MR) or glucocorticoid receptor (GR) in this enlargement. Ewes with single fetuses were randomly assigned at 120d gestation to one of four groups: maternal cortisol infusion (1mg kg-1 day-1, cortisol); maternal cortisol infusion with fetal intrapericardial infusion of the MR antagonist potassium canrenoate (600µg day-1; cortisol + MRa); maternal cortisol infusion with fetal intrapericardial infusion of the GR antagonist mifepristone (50µg day-1, cortisol + GRa); and maternal saline infusion (control). At 130 days gestation, fetal heart to body weight ratio and right (RV) and left ventricular (LV) free wall thickness were increased in the cortisol group compared to control group. Fetal hearts from the cortisol +MRa group weighed significantly less, with thinner LV, RV and interventricular septum walls, compared to the cortisol group. Fetal hearts from the cortisol + GRa group had significantly thinner RV walls than the cortisol group. Fetal arterial pressure and heart rate were not different among groups at 130 days. Picrosirius red staining of fetal hearts indicated that the increased size was not accompanied by cardiac fibrosis. These results suggest that physiologic increases in maternal cortisol late in gestation induce fetal cardiac enlargement via MR and, to a lesser extent, by GR, and indicate the enlargement is not secondary to an increase in fetal blood pressure or an increase in fibrosis within the fetal heart.

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