Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 17, Pages -Publisher
MDPI
DOI: 10.3390/ijms22179404
Keywords
polycystic ovary syndrome; vitamin D deficiency; rat model; estradiol relaxation; testosterone treatment
Funding
- Hungarian Hypertension Society
- Semmelweis University, Medical Faculty
- OTKA [K_125174, PD_132851]
- Fight for the Women's Hearts Medical Foundation
- Higher Education Institutional Excellence Programme of the Ministry of Human Capacities in Hungary of the Semmelweis University
Ask authors/readers for more resources
In a rat model, vitamin D deficiency was found to impair the vasoactive effect of estradiol, while short-term chronic hyperandrogenism did not have this effect. Additionally, vitamin D deficiency also affected the immunostaining of estrogen receptor and nitric oxide synthase.
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available