Document Detail


Regulation of placental growth by aldosterone and cortisol.
MedLine Citation:
PMID:  21068161     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
During pregnancy, trophoblasts grow to adapt the feto-maternal unit to fetal requirements. Aldosterone and cortisol levels increase, the latter being inactivated by a healthy placenta. By contrast, preeclamptic placental growth is reduced while aldosterone levels are low and placental cortisol tissue levels are high due to improper deactivation. Aldosterone acts as a growth factor in many tissues, whereas cortisol inhibits growth. We hypothesized that in preeclampsia low aldosterone and enhanced cortisol availability might mutually affect placental growth and function. Proliferation of cultured human trophoblasts was time- and dose-dependently increased with aldosterone (P < 0.04 to P < 0.0001) and inhibited by spironolactone and glucocorticoids (P < 0.01). Mineralo- and glucocorticoid receptor expression and activation upon agonist stimulation was verified by visualization of nuclear translocation of the receptors. Functional aldosterone deficiency simulated in pregnant mice by spironolactone treatment (15 μg/g body weight/day) led to a reduced fetal umbilical blood flow (P < 0.05). In rat (P < 0.05; R(2) = 0.2055) and human (X(2) = 3.85; P = 0.0249) pregnancy, placental size was positively related to plasma aldosterone. Autocrine production of these steroid hormones was excluded functionally and via the absence of specific enzymatic transcripts for CYP11B2 and CYP11B1. In conclusion, activation of mineralocorticoid receptors by maternal aldosterone appears to be required for trophoblast growth and a normal feto-placental function. Thus, low aldosterone levels and enhanced cortisol availability may be one explanation for the reduced placental size in preeclampsia and related disorders.
Authors:
Carine Gennari-Moser; Eliyahu V Khankin; Simone Schüller; Geneviève Escher; Brigitte M Frey; C-Bettina Portmann; Marc U Baumann; Andrea D Lehmann; Daniel Surbek; S Ananth Karumanchi; Felix J Frey; Markus G Mohaupt
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-11-10
Journal Detail:
Title:  Endocrinology     Volume:  152     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-24     Completed Date:  2011-01-31     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  263-71     Citation Subset:  AIM; IM    
Affiliation:
Department of Nephrology/Hypertension, University Hospital Bern, 3010 Berne, Switzerland.
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MeSH Terms
Descriptor/Qualifier:
Aldosterone / metabolism*
Animals
Cell Line
Female
Humans
Hydrocortisone / metabolism*
Mice
Placenta / growth & development*,  physiology*
Pregnancy
Rats
Chemical
Reg. No./Substance:
50-23-7/Hydrocortisone; 52-39-1/Aldosterone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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