Vascular endothelial growth factor, soluble fms-like tyrosine kinase 1 and genistein-induced changes in the vascular reactivity of rat's aorta

• Published in: The journal of obstetrics and gynaecology research 2015-02, Vol.41 (2), p.277-282
• Main Authors: Fernandez, Anne R., Husain, Ruby
• Format: Article
• Language: English
• Subjects: Animals; Aorta - drug effects; Endothelium - drug effects; genistein; Genistein - pharmacology; Male; Protein Kinase Inhibitors - pharmacology; rat's aorta; Rats; Rats, Sprague-Dawley; soluble fms-like tyrosine kinase 1; Tissue Culture Techniques; vascular endothelial growth factor; Vascular Endothelial Growth Factor A - pharmacology; Vascular Endothelial Growth Factor Receptor-1 - pharmacology; vascular reactivity; Vasodilation - drug effects
• ISSN: 1341-8076; 1447-0756
• DOI: 10.1111/jog.12511

Aim During preeclampsia (PE), the excessive circulation of soluble fms‐like tyrosine kinase 1 (sFLT1) hinders the vasodilatory effect of vascular endothelial growth factor (VEGF). This effect has been proven in vitro in the renal artery of rats. The endothelium of the blood vessels is also said to be dysfunctional in PE. Genistein has shown the ability to antagonize the vascular contractions caused by a wide range of contractile agents. We conducted vascular reactivity studies to demonstrate the effect of: (i) sFLT1 on the vasodilatory effect of VEGF; and (ii) genistein on the vasodilatory effect of VEGF and its effects on denuded blood vessels (dysfunctional endothelium). Material and Methods Isolated aortas of male Sprague–Dawley rats were exposed to sFLT1 or genistein and then subjected to increasing doses of VEGF. Results The presence of sFLT1 inhibited the vasodilatory effect of VEGF in the rats' aortas. Genistein significantly potentiated the vasodilatory effect by the VEGF. Conclusion The results suggest that genistein may help overcome the vasospasm in PE. It may be a promising therapeutic approach to PE.