HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: JOE-08-0022v1 198/2/419    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Google Scholar Articles by Reini, S. A Articles by Keller-Wood, M. PubMed PubMed Citation Articles by Reini, S. A Articles by Keller-Wood, M.

Department of Pharmacodynamics, College of Pharmacy, University of Florida, Box 100487, Gainesville, Florida 32610-0487, USA¹ Department of Physiology and Functional Genomics, College of Medicine, University of Florida, Gainesville, Florida 32610-0274, USA

(Correspondence should be addressed to M Keller-Wood; Email: kellerwd{at}cop.ufl.edu)

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 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 µg/day; cortisol+MRa); maternal cortisol infusion with fetal intrapericardial infusion of the GR antagonist (GRa) mifepristone (50 µg/day, cortisol+GRa); and maternal saline infusion (control). At 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.

This article has been cited by other articles:

				A. C. Montezano and R. M. Touyz Networking Between Systemic Angiotensin II and Cardiac Mineralocorticoid Receptors Hypertension, December 1, 2008; 52(6): 1016 - 1018. [Full Text] [PDF]