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Preimplantation antagonism of adrenomedullin action compromises fetoplacental development and reduces litter size. | LitMetric

Preimplantation antagonism of adrenomedullin action compromises fetoplacental development and reduces litter size.

Theriogenology

Department of Physiology Li Ka Shing Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.

Published: June 2012

AI Article Synopsis

  • Concentrations of adrenomedullin (ADM) rise in various areas during pregnancy, suggesting its role in reproductive processes.
  • Prior research indicates that blocking ADM receptors can hinder fetal-placental growth dynamics and affect litter size during post-implantation.
  • This study shows that inhibiting ADM actions during the preimplantation phase reduces litter size and promotes fetal resorption, emphasizing ADM's critical function in early pregnancy development.

Article Abstract

Concentrations of adrenomedullin (ADM) in circulation, the uterus, and corpora lutea (CL) increase during pregnancy. We previously reported a temporal-spatial pattern of ADM level and gene expression of Adm and its receptor components, from early pregnancy through midpregnancy to late pregnancy in rats. Two earlier reports using an in vivo model of ADM antagonism demonstrated the important roles of ADM in the post-implantation period. Treatment with ADM receptor blocker hADM22-52 starting from gestation Day 8 or Day 14 resulted in fetal-placental growth restriction and reduction in litter size. In this study, the endogenous ADM actions were abolished in the preimplantation period by infusing the antagonist for the ADM receptor (hADM22-52) with the osmotic (Alzet) pump from Days 1-4 of pregnancy. We inferred that ADM, acting through the ADM receptor, had critical roles during preimplantation, as brief inhibition of ADM action by hADM22-52 during this period reduced litter size by restricting placental growth and increasing fetal resorption in midpregnancy.

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Source
http://dx.doi.org/10.1016/j.theriogenology.2011.12.030DOI Listing

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