Journal article
Vasopressin: the missing link for preeclampsia?
American journal of physiology. Regulatory, integrative and comparative physiology, Vol.309(9), pp.R1062-R1064
11/01/2015
DOI: 10.1152/ajpregu.00073.2015
PMCID: PMC4666952
PMID: 25810383
Abstract
Preeclampsia is a devastating cardiovascular disorder of late pregnancy, affecting 5-7% of all pregnancies and claiming the lives of 76,000 mothers and 500,000 children each year. Various lines of evidence support a "tissue rejection" type reaction toward the placenta as the primary initiating event in the development of preeclampsia, followed by a complex interplay among immune, vascular, renal, and angiogenic mechanisms that have been implicated in the pathogenesis of preeclampsia beginning around the end of the first trimester. Critically, it remains unclear what mechanism links the initiating event and these pathogenic mechanisms. We and others have now demonstrated an early and sustained increase in maternal plasma concentrations of copeptin, a protein by-product of arginine vasopressin (AVP) synthesis and release, during preeclampsia. Furthermore, chronic infusion of AVP during pregnancy is sufficient to phenocopy essentially all maternal and fetal symptoms of preeclampsia in mice. As various groups have demonstrated interactions between AVP and immune, renal, and vascular systems in the nonpregnant state, elevations of this hormone are therefore positioned both in time (early pregnancy) and function to contribute to preeclampsia. We therefore posit that AVP represents a missing mechanistic link between initiating events and established midpregnancy dysfunctions that cause preeclampsia.
Details
- Title: Subtitle
- Vasopressin: the missing link for preeclampsia?
- Creators
- Jeremy A Sandgren - Departments of PharmacologySabrina M Scroggins - Obstetrics & GynecologyDonna A Santillan - Obstetrics & Gynecology, Center for Hypertension Research, University of Iowa, Iowa City, IowaEric J Devor - Obstetrics & GynecologyKatherine N Gibson-Corley - Pathology, andGary L Pierce - University of IowaCurt D Sigmund - University of IowaMark K Santillan - Obstetrics & Gynecology, Center for Hypertension Research, University of Iowa, Iowa City, Iowa; François M. Abboud Cardiovascular Research Center, University of Iowa, Iowa City, IowaJustin L Grobe - University of Iowa
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Regulatory, integrative and comparative physiology, Vol.309(9), pp.R1062-R1064
- DOI
- 10.1152/ajpregu.00073.2015
- PMID
- 25810383
- PMCID
- PMC4666952
- NLM abbreviation
- Am J Physiol Regul Integr Comp Physiol
- ISSN
- 1522-1490
- eISSN
- 1522-1490
- Publisher
- United States
- Grant note
- T32 GM067795 / NIGMS NIH HHS HL-062984 / NHLBI NIH HHS HL-084207 / NHLBI NIH HHS HL-048058 / NHLBI NIH HHS AG043722 / NIA NIH HHS T32 AI007260 / NIAID NIH HHS HL-098276 / NHLBI NIH HHS P01 HL084207 / NHLBI NIH HHS T32 AI-007260 / NIAID NIH HHS T32 GM-067795 / NIGMS NIH HHS
- Language
- English
- Date published
- 11/01/2015
- Academic Unit
- Molecular Physiology and Biophysics; Stead Family Department of Pediatrics; Pathology; Obstetrics and Gynecology; Neuroscience and Pharmacology; Health, Sport, and Human Physiology ; Ophthalmology and Visual Sciences
- Record Identifier
- 9983931815802771
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