Kivonat:
Background: polycystic ovary syndrome induces vascular damage of arteries, however, there is no data on the venous side. Aims: To clarify the effects of dihydrotestosterone (DHT)-induced polycystic ovary syndrome (PCOS) on both venous biomechanics and pharmacological reactivity in a rat model and to test the possible modulatory role of vitamin D3 (vitD). Methods and Results: The PCOS model was induced in female Wistar rats by DHT treatment (83 mug/day, subcutaneous pellet). After ten weeks, venous biomechanics, norepinephrine (NE)-induced contractility and acetylcholine relaxation were tested in saphenous veins segments from control, DHT- and DHT with vitD-treated animals using pressure angiography. Additionally, the e-NOS and COX-2 expressions 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, increased elasticity and resulted in vessels that were more relaxed. Although there was no difference in the endothelial dilation as tested using acetylcholine (ACh), the blocking effect of L-NG-nitroarginine methyl ester (L-NAME) was lower and was accompanied by a lowered COX-2 expression in the endothelium after the DHT treatment. VitD supplementation reversed all of these alterations. The eNOS expression did not differ between the three groups. Conclusion(s): The hyperandrogenic state resulted in thicker but less flexible vein walls. These veins showed the early remodelling and altered vasorelaxant mechanisms similarly to varicose veins. These alterations caused by the chronic DHT treatment were partially reversed by concomitant vitD administration.
