Blood Pressure, Renal Arterial Function and Oxidative-Nitrative Stress in a Rat Model of Polycystic Ovary Syndrome

Objective: Polycystic ovary syndrome (PCOS), a prevalent endocrine disorder in women, is associated with elevated cardiovascular risk and vitamin D deficiency. This study evaluates blood pressure, renal arterial function and oxidative stress in a rat PCOS model, also exploring the impact of vitamin D supplementation. Assessing mean arterial blood pressure under anesthesia, renal arterial function and oxidative stress in a hyperandrogenic rat model, and the effectiveness of vitamin D substitution. Design and method: Thirty-two adolescent female Wistar rats were randomly assigned into four groups. Eight rats received no treatment (controls, C), eight received weekly Vitamin D per os (140 IU/100 g body weight, group D), eight received cutaneous testosterone daily (3.3 mg/100 g, T), and eight received Vitamin D and testosterone together (T+D). In the eighth week of the treatment, rats were anaesthetized with urethane, and blood pressure (MABP) was measured. The isolated renal arterial rings were cut into 3-4 mm long segments for wire myography. Other segments were formaldehyde-fixed and paraffin-embedded for histological evaluations. By immunohistochemical methods, we assessed the oxidative stress marker 4-hydroxynoneal (HNE) and poly(ADP-ribose) polymerase activation shown by nuclear poly(ADP-ribose) polymer (PAR). Results: MABP was lower in hyperandrogenic rats, which was not altered by Vitamin D supplementation. Phenylephrine-induced contraction (Phe) in 10-9-10-7 M concentrations was identical in all groups; however, 10-6 M Phe caused a lower contraction in D and T rats (54.4± 21% and 41.9±20% vs. C: 72.78±8% and T+D: 69.68±21%. p<0.05) compared to controls and double treated animals. Endothelium-mediated relaxation did not differ between groups. PAR staining was also identical, but HNE staining showed a tendency for increment in group T (p=0.12) but not in T+D. Conclusions: The decreased mean arterial pressure is likely the result of the compromised sensitivity to alpha1-adrenergic stimulus. The reduced reactivity of the renal artery may influence the activity of the renin-angiotensin-aldosterone system (RAAS). By normalizing the phenylephrine-induced contraction, Vitamin D supplementation might restore RAAS, thus blood pressure regulation.