Abstract
We examined the vasoactive effect of estradiol in a rat model of early PCOS and the influence of vitamin D deficiency (VDD). We created a model of chronic hyperandrogenism and VDD in adolescent female Wistar rats (N = 46) with four experimental groups: vitamin D supplemented (T-D+), VDD (T-D-), hyperandrogenic and vitamin D supplemented (T+D+), and hyperandrogenic and VDD (T+D-). T+ groups received an 8-week-long transdermal Androgel treatment, D-animals were on vitamin D-reduced diet and D+ rats were supplemented orally with vitamin D3. Estrogen-induced vasorelaxation of thoracic aorta segments were measured with a wire myograph system with or without the inhibition of endothelial nitric oxide synthase (eNOS) or cyclooxygenase-2 (COX-2). The distribution of estrogen receptor (ER), eNOS and COX-2 in the aortic wall was assessed by immunohistochemistry. VDD aortas showed significantly lower estradiol-induced relaxation independently of androgenic status that was further decreased by COX-2 inhibition. COX-2 inhibition failed to alter vessel function in D+ rats. Inhibition of eNOS abolished the estradiol-induced relaxation in all groups. Changes in vascular function in VDD were accompanied by significantly decreased ER and eNOS staining. Short-term chronic hyperandrogenism failed to, but VDD induced vascular dysfunction, compromised estrogen-dependent vasodilatation and changes in ER and eNOS immunostaining.
Highlights
IntroductionPolycystic ovary syndrome (PCOS) affects approximately 2–20% of women in reproductive age which makes it the most prevalent endocrine disease of this cohort [1]
Polycystic ovary syndrome (PCOS) affects approximately 2–20% of women in reproductive age which makes it the most prevalent endocrine disease of this cohort [1].PCOS can be genetically determined but it depends greatly on environmental influences.Diagnosis of PCOS relies on the Rotterdam criteria: two of the following three should be 4.0/).observed: clinical or biochemical hyperandrogenism, ovulatory dysfunction and polycystic morphology of the ovaries [2]
We were unable to show a significant increase in COX-2 staining in vitamin D deficiency (VDD)
Summary
Polycystic ovary syndrome (PCOS) affects approximately 2–20% of women in reproductive age which makes it the most prevalent endocrine disease of this cohort [1]. Observed: clinical or biochemical hyperandrogenism, ovulatory dysfunction and polycystic morphology of the ovaries [2]. The early appearance of vascular dysfunction in the pathogenesis of the disease may contribute to the increased CV risk [3]. Deterioration of endothelium-dependent vasorelaxation can be the first sign of vascular dysfunction [5]. The lower prevalence of hypertension in women of reproductive age might be related to the vasorelaxant effect of estrogen [6], and the higher risk of hypertension in women with PCOS could be caused by the impairment of this mechanism [7]
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