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Hum. Reprod. Advance Access published online on November 25, 2005
Human Reproduction, doi:10.1093/humrep/dei399
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© The Author 2005. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received June 10, 2005
Revised September 8, 2005
Accepted October 12, 2005

Article

Aortic function is compromised in a rat model of polycystic ovary syndrome

Kalpana Lakhani 1, Wenxuan Yang 2, Audrey Dooley 3, Essam El-Mahdi 4, Maryse Sundaresan 5, Susan McLellan 6, Richard Bruckdorfer 3, Andrew Leonard 4, Alexander Seifalian 2, and Paul Hardiman 4 *

1 Ultrasound Department, North Middlesex Hospital, London
2 Department of Surgery, Royal Free and University College Medical School, University College London
3 Department of Biochemistry and Molecular Biology, Royal Free and University College Medical School, University College London
4 Academic Department of Obstetrics and Gynaecology, Royal Free and University College Medical School, University College London
5 Department of Histopathology, North Middlesex Hospital, London
6 Department of Chemical Pathology, Royal Free and University College Medical School, University College London

* To whom correspondence should be addressed.
Paul Hardiman, E-mail: p.hardiman{at}medsch.ucl.ac.uk


  Abstract

BACKGROUND: Arterial mechanical parameters are modified in women with polycystic ovary syndrome (PCOS), before and during pregnancy. This study tested the hypothesis that aortic mechanics and endothelial function are modified in the mifepristone-treated rat model of PCOS. METHODS: Female rats injected daily with mifepristone or vehicle for 7-9 days were assessed by ultrasound to allow estimation of aortic stiffness index and compliance. The influence of acetylcholine (ACh) and sodium nitroprusside (SNP) on dissected phenylephrine-contracted aortic rings was assessed. RESULTS: Aortic compliance was reduced by 67% in mifepristone-treated rats versus controls (P < 0.05), while stiffness index was increased 2.3-fold (P < 0.02). ACh-induced dilation was less in aortic rings from mifepristone-treated rats (P = 0.022) and was less sensitive to the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (P < 0.001), while SNP-induced dilation was greater (P = 0.001). CONCLUSIONS: Aortic mechanics in vivo and endothelial function in vitro were consistently perturbed in mifepristone-treated rats. Aortic ring behaviour suggested that NO release was depressed or degradation elevated, with a compensatory increase in NO sensitivity and/or activation of a non-NO-mediated relaxation mechanism. The mifepristone-treated rat is a valid model for investigation of the vascular deficits seen in PCOS.

Keywords: animal model/polycystic ovaries/ultrasound/vascular system.
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