Lower-limb veins are thicker and vascular reactivity is decreased in a rat PCOS model: concomitant vitamin D 3 treatment partially prevents these changes

Polycystic ovary syndrome (PCOS) causes vascular damage to arteries; however, there are no data for its effect on veins. Our aim was to clarify the effects of dihydrotestosterone (DHT)-induced PCOS both on venous biomechanics and on pharmacological reactivity in a rat model and to test the possible...

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Published inAmerican journal of physiology. Heart and circulatory physiology Vol. 307; no. 6; pp. H848 - H857
Main Authors Várbíró, Szabolcs, Sára, Levente, Antal, Péter, Monori-Kiss, Anna, Tőkés, Anna-Mária, Monos, Emil, Benkő, Rita, Csibi, Noémi, Szekeres, Maria, Tarszabo, Robert, Novak, Agnes, Paragi, Péter, Nádasy, György L.
Format Journal Article
LanguageEnglish
Published 15.09.2014
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Summary:Polycystic ovary syndrome (PCOS) causes vascular damage to arteries; however, there are no data for its effect on veins. Our aim was to clarify the effects of dihydrotestosterone (DHT)-induced PCOS both on venous biomechanics and on pharmacological reactivity in a rat model and to test the possible modulatory role of vitamin D 3 (vitD). PCOS was induced in female Wistar rats by DHT treatment (83 μg/day, subcutaneous pellet). After 10 wk, the venous biomechanics, norepinephrine (NE)-induced contractility, and acetylcholine-induced relaxation were tested in saphenous veins from control animals and from animals treated with DHT or DHT with vitD using pressure angiography. Additionally, the expression levels of endothelial nitric oxide synthase (eNOS) and cyclooxygenase (COX-2) were measured using immunohistochemistry. Increased diameter, wall thickness, and distensibility as well as decreased vasoconstriction were detected after the DHT treatment. Concomitant vitD treatment lowered the mechanical load on the veins, reduced distensibility, and resulted in vessels that were more relaxed. Although there was no difference in the endothelial dilation tested using acetylcholine (ACh), the blocking effect of N G -nitro-l-arginine methyl ester (l-NAME) was lower and was accompanied by lower COX-2 expression in the endothelium after the DHT treatment. Supplementation with vitD prevented these alterations. eNOS expression did not differ among the three groups. We conclude that the hyperandrogenic state resulted in thicker vein walls. These veins showed early remodeling and altered vasorelaxant mechanisms similar to those of varicose veins. Alterations caused by the chronic DHT treatment were prevented partially by concomitant vitD administration.
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.01024.2013