| Oxidative stress contributes to soluble fms-like tyrosine kinase-1 induced vascular dysfunction in pregnant rats. | |
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MedLine Citation:
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PMID: 19265787 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Recent evidence indicates that both increased oxidative stress and an altered balance between pro- and anti-angiogenic factors such as vascular-endothelial growth factor (VEGF) and the soluble VEGF receptor (sFlt-1) contribute to endothelial dysfunction in preeclampsia. We hypothesized that chronic infusion of sFlt-1 to mimic the increase observed in preeclamptic patients would reduce plasma VEGF concentrations, increase blood pressure (BP) and vascular superoxide levels, and cause endothelial dysfunction in the pregnant rat. METHODS: Recombinant sFlt-1 was infused (500 ng/h) during days 13-18 of pregnancy. BP, fetal and placental weight, oxidative stress and vessel vasorelaxation were determined on day 18 of pregnancy. RESULTS: Plasma sFlt-1 concentrations (299 +/- 33 vs. 100 +/- 16 pg/ml; P < 0.01) and BP (117 +/- 6 vs. 98 +/- 4 mm Hg; P < 0.01) were increased, while plasma-free VEGF concentrations (570 +/- 77 vs. 780 +/- 48 pg/ml; P < 0.01) were decreased when compared to vehicle infused dams. sFlt-1 rats had smaller fetuses (1.3 +/- 0.03 vs. 1.5 +/- 0.04 g, P < 0.01) and placentas (0.41 +/- 0.01 vs. 0.47 +/- 0.02 g; P < 0.05). Placental (180 +/- 66 vs. 24 +/- 2.3 RLU/min/mg; P < 0.05) and vascular (34 +/- 8 vs. 12 +/- 5 RLU/min/mg; P < 0.05) superoxide production was increased in the sFlt-1 compared to vehicle infused rats. Vasorelaxation to acetylecholine (ACh) and sodium nitroprusside (SNP) were both decreased (P < 0.05) in the sFlt-1 infusion group compared to the vehicle and this decrease was attenuated (P < 0.05) by the superoxide scavenger Tiron. CONCLUSION: These data indicate elevated maternal sFlt-1 and decreased VEGF concentrations results in increased oxidative stress that contributes to vascular dysfunction during pregnancy. |
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Authors:
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Jason P Bridges; Jeffrey S Gilbert; Drew Colson; Sara A Gilbert; Matthew P Dukes; Michael J Ryan; Joey P Granger |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2009-03-05 |
Journal Detail:
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Title: American journal of hypertension Volume: 22 ISSN: 1941-7225 ISO Abbreviation: Am. J. Hypertens. Publication Date: 2009 May |
Date Detail:
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Created Date: 2009-04-23 Completed Date: 2009-05-28 Revised Date: 2013-06-02 |
Medline Journal Info:
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Nlm Unique ID: 8803676 Medline TA: Am J Hypertens Country: United States |
Other Details:
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Languages: eng Pagination: 564-8 Citation Subset: IM |
Affiliation:
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Department of Physiology and the Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Blood Pressure / drug effects Female Fetal Growth Retardation / etiology Nitroprusside / pharmacology Oxidative Stress / physiology* Pregnancy Pregnancy, Animal / blood, physiology Rats Superoxides / metabolism Vascular Endothelial Growth Factor Receptor-1 / physiology* Vasodilation / drug effects |
| Grant Support | |
ID/Acronym/Agency:
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HL51971/HL/NHLBI NIH HHS; HL85907/HL/NHLBI NIH HHS; HL90269/HL/NHLBI NIH HHS; P01 HL051971-165259/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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11062-77-4/Superoxides; 15078-28-1/Nitroprusside; EC 2.7.10.1/Flt1 protein, rat; EC 2.7.10.1/Vascular Endothelial Growth Factor Receptor-1 |
| Comments/Corrections | |
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