Testosterone-induced PCOS and vitamin D deficiency in Wistar rats resulted in dysfunctional vascular responses, including increased angiotensin II-induced contraction in PCOS females.
Does vitamin D deficiency and supplementation affect carotid artery vascular reactivity differently in male and female Wistar rats with and without testosterone-induced PCOS?
Vitamin D deficiency and PCOS both result in dysfunctional vascular responses in the carotid artery, with significant gender differences in reactivity.
The negative cardiovascular effects of polycystic ovary syndrome (PCOS) and vitamin D deficiency (VDD) have been discussed previously; however, the sex differences between PCOS females and males are not yet known. Our aim was to investigate the effect of PCOS and VDD in the carotid artery of male and female Wistar rats. Females were treated with transdermal testosterone (Androgel) for 8 weeks, which caused PCOS. VDD and vitamin D supplementation were accomplished via diet. The carotid arteries' contraction and relaxation were examined using myography. Receptor density was investigated using immunohistochemistry. In PCOS females, angiotensin receptor density, angiotensin II-induced contraction, androgen receptor optical density, and testosterone-induced relaxation increased. The increased contractile response may increase cardiovascular vulnerability in women with PCOS. As an effect of VDD, estrogen receptor density increased in all our groups, which probably compensated for the reduced relaxation caused by VDD. Testosterone-induced relaxation was decreased as a result of VDD in males and non-PCOS females, whereas this reduction was absent in PCOS females. Male sex is associated with increased contraction ability compared with non-PCOS and PCOS females. VDD and Androgel treatment show significant gender differences in their effects on carotid artery reactivity. Both VDD and PCOS result in a dysfunctional vascular response, which can contribute to cardiovascular diseases.
Süli et al. (Tue,) conducted a other in Polycystic ovary syndrome (PCOS) and vitamin D deficiency. Transdermal testosterone (Androgel) and Vitamin D deficiency/supplementation vs. Males and non-PCOS females was evaluated on Carotid artery contraction and relaxation and receptor density. Testosterone-induced PCOS and vitamin D deficiency in Wistar rats resulted in dysfunctional vascular responses, including increased angiotensin II-induced contraction in PCOS females.