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Uterine vascular function in a transgenic preeclampsia rat model

Item Type:Article
Title:Uterine vascular function in a transgenic preeclampsia rat model
Creators: Verlohren, S. ORCID logoORCID: https://orcid.org/0000-0003-3507-8636, Niehoff, M., Hering, L., Geusens, N., Herse, F. ORCID logoORCID: https://orcid.org/0000-0002-9305-8134, Tintu, A.N., Plagemann, A., le Noble, F. ORCID logoORCID: https://orcid.org/0000-0001-6195-7672, Pijnenborg, R., Mueller, D.N. ORCID logoORCID: https://orcid.org/0000-0003-3650-5644, Luft, F.C. ORCID logoORCID: https://orcid.org/0000-0002-8635-1199, Dudenhausen, J.W., Gollasch, M. ORCID logoORCID: https://orcid.org/0000-0003-2797-1934 and Dechend, R. ORCID logoORCID: https://orcid.org/0000-0001-6636-3080
Abstract:We investigated intrauterine growth restriction, endothelial function, and uterine artery blood flow characteristics in a transgenic preeclampsia rat model with an activated renin-angiotensin system. We compared preeclamptic Sprague-Dawley (SD-PE) rats with normal pregnant Sprague-Dawley and nonpregnant Sprague-Dawley rats. We used transabdominal ultrasound and found that SD-PE rat embryos developed intrauterine growth restriction. Isolated uterine arteries from SD-PE rats incubated with phenylephrine exhibited an increased contractile response, whereas a single high dose of acetylcholine resulted in an impaired vasorelaxation compared with controls. Incremental acetylcholine doses increased relaxation of SD-PE vessels at low acetylcholine doses but caused a paradoxical contraction at higher acetylcholine doses. Indomethacin and a thromboxane-receptor antagonist (SQ 29,548) blocked this effect, suggesting maternal prostanoid-dependent endothelial dysfunction. SD-PE rats had a decreased prostacyclin (6-keto-prostaglandin F1alpha):thromboxane ratio in the serum compared with normal pregnant Sprague-Dawley rats or nonpregnant Sprague-Dawley. Surprisingly, the Doppler resistance index decreased during pregnancy in SD-PE compared with normal pregnant Sprague-Dawley rats, suggesting unimpaired uteroplacental flow in the uterine artery. Umbilical flow was unchanged with absent end-diastolic flow in all of the groups. Renin-angiotensin system activation-induced preeclampsia is associated with altered placentation, modified resistance index, and endothelial dysfunction. A disturbed prostacyclin:thromboxane ratio could be an important mediator.
Keywords:Preeclampsia, Uterine artery, Intrauterine growth restriction, Endothelial dysfunction, Doppler ultrasound, Animals, Rats
Source:Hypertension
ISSN:0194-911X
Publisher:American Heart Association
Volume:51
Number:2
Page Range:547-553
Date:February 2008
Official Publication:https://doi.org/10.1161/HYPERTENSIONAHA.107.103176
PubMed:View item in PubMed

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