Altered insulin induced relaxation of aortic rings in a dihydrotestosterone induced rodent model of polycystic ovary syndrome

Insulin-dependent vasorelaxation in aortic rings in a PCOS rat model is decreased (both NO-dependent or independent), and vitamin D treatment can improve only the NO-independent model.


Gabriella Masszi, M.D., Anna Buday, Agnes Novak, Eszter M. Horvath, M.D., Ph.D., Robert Tarszabo, Levente Sara, M.D., Csaba Revesz, M.D., Rita Benkő, Ph.D., Gyorgy L. Nadasy, M.D., Ph.D., Zoltán Benyó, M.D., Ph.D., D.M.Sc., Péter Hamar, M.D., Ph.D., D.M.Sc., Szabolcs Varbiro, Ph.D.

Volume 99, Issue 2, Pages 573-578, February 2013



To clarify the effects of dihydrotestosterone (DHT)-induced polycystic ovary syndrome (PCOS) on the insulin-dependent vasodilatation of the thoracic aorta and the role of vitamin D in a rat model.


Controlled experimental animal study.




Thirty adolescent female Wistar rats.


The PCOS model was induced by 10 weeks of DHT treatment (83 μg/day). Half of the DHT-treated animals received vitamin D (120 ng/bwkg/week) in parallel.

Main Outcome Measures:

The aortic rings of the control, DHT and DHT plus vitamin D3-treated animals (n=10-10) were isolated. The insulin-dependent vasodilation of the isolated aortic rings was compared between rings in Krebs-Ringer solution and under blockade of NO-synthase or cyclooxygenase.


The insulin-dependent vasorelaxation decreased in both DHT-treated groups independently of the vitamin D treatment; NO-dependent and independent relaxations were both impaired. In response to prostanoid, vasoconstriction was increased following DHT treatment. The NO-independent relaxation was partially improved by vitamin D treatment, which was neutralized by increased prostanoid-dependent vasoconstriction.


Previously, we found that vitamin D3 treatment prevented systemic insulin resistance; however, in this study, we did not detect any influence on the vascular insulin resistance of the aorta that was induced by DHT treatment. Consequently, controlling insulin resistance with vitamin D3 alone did not resolve the aortic endothelial dysfunction caused by the hyperandrogenic state.

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