NDLI: Cardiac corticosteroid receptors mediate the enlargement of the ovine fetal heart induced by chronic increases in maternal cortisol.

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Cardiac corticosteroid receptors mediate the enlargement of the ovine fetal heart induced by chronic increases in maternal cortisol.

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Cardiac corticosteroid receptors mediate the enlargement of the ovine fetal heart induced by chronic increases in maternal cortisol.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Reini, Seth A. Dutta, Garima Wood, Charles E. Keller-Wood, Maureen
Description	Country affiliation: United States Author Affiliation: Reini SA ( Department of Pharmacodynamics, College of Pharmacy, University of Florida, Box 100487, Gainesville, Florida 32610-0487, USA.)
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 receptor (MR) or glucocorticoid receptor (GR) in this enlargement. Ewes with single fetuses were randomly assigned at approximately 120 days of gestation to one of four groups: maternal cortisol infusion (1 mg/kg per day, cortisol); maternal cortisol infusion with fetal intrapericardial infusion of the MR antagonist (MRa) potassium canrenoate (600 microg/day; cortisol+MRa); maternal cortisol infusion with fetal intrapericardial infusion of the GR antagonist (GRa) mifepristone (50 microg/day, cortisol+GRa); and maternal saline infusion (control). At approximately 130 days of gestation, fetal heart to body weight ratio and right ventricular (RV) and left ventricular (LV) free wall thicknesses were increased in the cortisol group when compared with control group. Fetal hearts from the cortisol+MRa group weighed significantly less, with thinner LV, RV, and interventricular septum walls, when compared with 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 in late gestation induce fetal cardiac enlargement via MR and, to a lesser extent, by GR, and indicate that the enlargement is not secondary to an increase in fetal blood pressure or an increase in fibrosis within the fetal heart.
File Format	HTM / HTML
ISSN	00220795
e-ISSN	14796805
DOI	10.1677/JOE-08-0022
Journal	Journal of Endocrinology
Issue Number	2
Volume Number	198
Language	English
Publisher	BioScientifica
Publisher Date	2008-08-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Endocrinology Anti-inflammatory Agents Pharmacology Cardiomegaly Chemically Induced Fetal Heart Drug Effects Hydrocortisone Receptors, Steroid Metabolism Adrenocorticotropic Hormone Blood Animals Canrenoic Acid Pathology Administration & Dosage Immunohistochemistry Mifepristone Mineralocorticoid Receptor Antagonists Pregnancy Receptors, Glucocorticoid Antagonists & Inhibitors Receptors, Mineralocorticoid Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Endocrinology, Diabetes and Metabolism Endocrinology

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Cardiac Corticosteroid Receptors Mediate the Enlargement of the Ovine Fetal Heart Induced by Chronic Increases in Maternal Cortisol

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