SFlt-1 elevates blood pressure by augmenting endothelin-1-mediated vasoconstriction in mice

Scavenging of vascular endothelial growth factor (VEGF) elevates blood pressure (BP) in patients receiving anti-angiogenic therapy. Similarly, inhibition of circulation VEGF by its soluble receptor fms-like tyrosine kinase-1 (sFlt-1) underlies BP elevation in pre-eclampsia. Both phenotypes are chara...

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Veröffentlicht in:	PloS one 2014-03, Vol.9 (3), p.e91897
Hauptverfasser:	Amraoui, Fouad, Spijkers, Léon, Hassani Lahsinoui, Hajar, Vogt, Liffert, van der Post, Joris, Peters, Stephan, Afink, Gijs, Ris-Stalpers, Carrie, van den Born, Bert-Jan
Format:	Artikel
Sprache:	eng
Schlagworte:	Angiogenesis Animals Arteries Aspirin Biology Biology and Life Sciences Blood Blood circulation Blood pressure Blood Pressure - drug effects Carotid Arteries - drug effects Carotid Arteries - physiology Comparative analysis Contractility Contraction COX-2 inhibitors Endothelin Endothelin 1 Endothelin-1 - metabolism Endothelium Flexible manufacturing systems Gene expression Gene Expression Regulation - drug effects Hypertension Indomethacin Inhibition Inhibitors Isometric Kidneys Kinases Laboratories Male Medical research Medicine Medicine and Health Sciences Mice Mice, Inbred C57BL Nitric oxide Plasma Pre-eclampsia Preeclampsia Pregnancy Prostaglandin endoperoxide synthase Protein-tyrosine kinase Protein-tyrosine kinase receptors Receptors, Endothelin - genetics RNA, Messenger - genetics RNA, Messenger - metabolism Rodents Segments Signaling Solubility Thromboxane A2 Tyrosine Vascular endothelial growth factor Vascular Endothelial Growth Factor A - antagonists & inhibitors Vascular Endothelial Growth Factor Receptor-1 - chemistry Vascular Endothelial Growth Factor Receptor-1 - pharmacology Vasoconstriction Vasoconstriction - drug effects Veins & arteries
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Zusammenfassung:	Scavenging of vascular endothelial growth factor (VEGF) elevates blood pressure (BP) in patients receiving anti-angiogenic therapy. Similarly, inhibition of circulation VEGF by its soluble receptor fms-like tyrosine kinase-1 (sFlt-1) underlies BP elevation in pre-eclampsia. Both phenotypes are characterized by augmented production of endothelin-1 (ET-1), suggesting a role for ET-1 in anti-angiogenic hypertension. We aimed to assess the effect of VEGF inhibition on ET-1-induced contractility and downstream ET-1 signaling. Male C57BL/6N mice were treated with either sFlt-1 or vehicle and BP was assessed via tail-cuff. Mean arterial pressure of sFlt-1-treated mice markedly increased compared to vehicle-treated controls (N = 11-12, p
ISSN:	1932-6203 1932-6203
DOI:	10.1371/journal.pone.0091897