Dean of the Medical Faculty, Semmelweis University
(PD_132851)
(K-125174) Támogató: Nemzeti Kutatás, Fejlesztés és Innovációs Iroda
(Molecular Biology Thematic Programme of Semmelweis University)
(Fight for the Women’s Hearts Medical Foundation)
Hungarian Hypertension Society
Szakterületek:
Élettan és orvostechnológia
Endokrinológia
Polycystic ovary syndrome (PCOS) is associated with elevated cardiovascular risk.
Early vascular dysfunction may lead to the development of cardiovascular disease in
PCOS. Vitamin D deficiency (VDD) is a common comorbidity of PCOS that contributes
to the pathogenesis of the disease and its complications. Both PCOS and VDD are accompanied
by increased oxidative stress that may be involved in the arising vascular dysfunction.
We aimed to investigate the role of vitamin D status on aortic function. PCOS was
induced by an 8-week-long transdermal testosterone treatment of female rats, and low
and adequate vitamin D status was achieved by dietary means. Contraction and relaxation
abilities of isolated aortic segments were measured by myograph. Resorcin-fuchsin
staining and immunohistochemical labeling of 3-nitrotyrosine were performed. No difference
was shown in the norepinephrine-induced contraction of the aortas of different groups,
whereas we detected reduced acetylcholine- and insulin-evoked relaxation in VDD groups.
A lower level of resorcin-fuchsin staining and elevated 3-nitrotyrosine immunostaining
was observed in VDD. In our study, we demonstrated early endothelial dysfunction in
VDD PCOS rat model. Vitamin D supplementation could prevent vascular disturbances,
while VDD itself damaged endothelium-dependent vasorelaxation and induced nitrative
stress.