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Influence of maternal hypothyroidism in fetal cardiac Renin‐Angiotensin System (RAS)
Author(s) -
Lino Caroline Antunes,
Shibata Caroline Emy Rodrigues,
BarretoChaves Maria Luiza
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.544.1
Subject(s) - fetus , endocrinology , medicine , offspring , angiotensin ii , gestational age , thyroid , renin–angiotensin system , hormone , embryogenesis , pregnancy , lung , embryo , biology , blood pressure , genetics , microbiology and biotechnology
Objective Thyroid hormones (TH) are critical for organogenesis and fetal development. Similarly, the RAS has also been implicated in embryogenesis. However, the possible influence exerted by maternal hypothyroidism during the pregnancy in cardiac RAS of embryos is unknown. The aim of this study was to analyze the maternal hypothyroidism effect in the expression of some RAS components in fetal heart at embryonic day 20 (ED 20). Methods Females Wistar rats were mating with 12 weeks of age. At gestational day 9, the dams were divided into 2 groups. The control received water and hypothyroid (hypo) group received water with Metimazol (0.02%). Dams and offspring were killed at ED20. Total body, heart, lung and renal weights of fetuses were evaluated. Western Blotting was used to evaluate AT1, AT2 and Ang I/II expression levels in fetal heart. Data were expressed as mean±SD and were analyzed using analysis of variance. Values of P<0.05 were considered statistically significant (n=5). Results Total body, lung and renal weights were decreased in embryos of hypo group. However, AT1, AT2 and Ang I/II expression levels in fetal heart in hypo group were not different compared to that observed in control. Conclusion Although RAS is modulated during the embryogenesis period, the induction of maternal hypothyroidism was not able to promote alteration on fetal cardiac expression levels of RAS components at ED 20.