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Background/objectives: Both hyperandrogenism (HA) and vitamin D deficiency (VDD) can separately lead to impaired vascular reactivity and ovulatory dysfunction in fertile females. The aim was to examine the early interactions of these states in a rat model of PCOS., Methods: Four-week-old adolescent female rats were divided into four groups: vitamin D (VD)-supplemented ( n = 12); VD-supplemented and testosterone-treated ( n = 12); VDD- ( n = 11) and VDD-and-testosterone-treated ( n = 11). Animals underwent transdermal testosterone treatment for 8 weeks. Target VD levels were achieved with oral VD supplementation and a VD-free diet. Estrous cycles were followed by vaginal smear, and quantitative histomorphometric measurements of the ovaries were also taken. In the 8th week, testosterone- and estrogen-induced relaxation of coronary arterioles was examined with pressure angiography. Estrogen receptor (ER) density and oxidative and nitrative stress parameters (Poly-(ADP-Ribose)-Polymerase and 3-nitrotyrosine) in the vessel wall were investigated with immunohistochemistry., Results: VDD caused impaired estrous cycles, and testosterone caused anovulatory cycles (the cycles were stopped at the diestrous phase). VDD combined with testosterone treatment resulted in reduced testosterone and estrogen vasorelaxation, lower ER density, and higher oxidative and nitrative stress in the vessel wall., Conclusions: PCOS with vitamin D deficiency may be associated with increased oxidative-nitrative stress in coronary arterioles. This oxidative and nitrative stress, potentially caused by hyperandrogenism and/or vitamin D deficiency, could impair estrogen-induced relaxation of the coronary arterioles, possibly by decreasing NO bioavailability and disrupting the estrogen-induced relaxation pathway.

Background: Vitamin D deficiency (VDD) may be considered an independent cardiovascular (CV) risk factor, and it is well known that CV risk is higher in males. Our goal was to investigate the pharmacological reactivity and receptor expression of intramural coronary artery segments of male rats in cases of different vitamin D supply., Methods: Four-week-old male Wistar rats were divided into a control group ( n = 11) with optimal vitamin D supply (300 IU/kgbw/day) and a VDD group ( n = 11, <0.5 IU/kgbw/day). After 8 weeks of treatment, intramural coronary artery segments were microprepared, their pharmacological reactivity was examined by in vitro microangiometry, and their receptor expression was investigated by immunohistochemistry., Results: Thromboxane A 2 (TXA 2 )-agonist induced reduced vasoconstriction, testosterone (T) and 17-β-estradiol (E2) relaxations were significantly decreased, a significant decrease in thromboxane receptor (TP) expression was shown, and the reduction in estrogen receptor-α (ERα) expression was on the border of significance in the VDD group., Conclusions: VD-deficient male coronary arteries showed deteriorated pharmacological reactivity to TXA 2 and sexual steroids (E2, T). Insufficient vasoconstrictor capacity was accompanied by decreased TP receptor expression, and vasodilator impairments were mainly functional. The decrease in vasoconstrictor and vasodilator responses results in narrowed adaptational range of coronaries, causing inadequate coronary perfusion that might contribute to the increased CV risk in VDD.

Background: Several reports prove interconnection between vitamin D (VD) deficiency and increased cardiovascular risk. Our aim was to investigate the effects of VD status on biomechanical and oxidative-nitrative (O-N) stress parameters of coronary arterioles in rats., Methods: 4-week-old male Wistar rats were divided into a control group (11 animals) with optimal VD supply (300 IU/kgbw/day) and a VD-deficient group (11 animals, <5 IU/kg/day). After 8 weeks, coronary arteriole segments were prepared. Geometrical, elastic, and biomechanical characteristics were measured by in vitro arteriography. O-N stress markers were investigated by immunohistochemistry., Results: Inner radius decreased; wall thickness and wall-thickness/lumen diameter ratio increased; tangential wall stress and elastic modulus were reduced in VD-deficient group. No difference could be found in wall-cross-sectional area, intima-media area %. While the elastic elements of the vessel wall decreased, the α-smooth muscle actin (α-SMA) immunostaining intensity showed no changes. Significant elevation was found in the lipid peroxidation marker of 4-hidroxy-2-nonenal (HNE), while other O-N stress markers staining intensity (poly(ADP)ribose, 3-nitrotyrosine) did not change., Conclusions: Inward eutrophic remodeling has developed. The potential background of these impairments may involve the initial change in oxidative damage markers (HNE). These mechanisms can contribute to the increased incidence of the cardiovascular diseases in VD deficiency.

Hyperandrogenism is a risk factor of cerebrovascular diseases as androgens can alter markedly the regulation of cerebrovascular tone. We examined the combined impact of androgen excess and vitamin D deficiency (VDD), a common co-morbidity in hyperandrogenic disorders, on remodeling and testosterone-induced vascular responses of anterior cerebral arteries (ACA) in order to evaluate the interplay between androgens and VDD in the cerebral vasculature. Male and female Wistar rats were either fed with vitamin D deficient or vitamin D supplemented diet. Half of the female animals from both groups received transdermal testosterone treatment. After 8 weeks, vessel lumen, wall thickness and testosterone-induced vascular tone of isolated ACA were determined using pressure microangiometry and histological examination. Androgen receptor protein expression in the wall of cerebral arteries was examined using immunohistochemistry. In female rats only combined VDD and testosterone treatment decreased the lumen and increased the wall thickness of ACA. In males, however VDD by itself was able to decrease the lumen and increase the wall thickness. Vascular reactivity showed similar alterations: in females, testosterone constricted the ACA only after combined VDD and hyperandrogenism, whereas in males VDD resulted in increased testosterone-induced contractions in spite of decreased androgen receptor expression. In conclusion, a marked interplay between hyperandrogenism and VDD results in inward remodeling and enhanced testosterone-induced constrictions of cerebral arteries, which might compromise the cerebral circulation and thus, increase the risk of stroke in the long term. In addition, the early cerebrovascular manifestation of VDD appears to require androgen excess and thus, depends on gender., Competing Interests: The authors have declared that no competing interests exist.

Background and Purpose: Vitamin D deficiency (VDD) is a global health problem, which can lead to several pathophysiological consequences including cardiovascular diseases. Its impact on the cerebrovascular system is not well understood. The goal of the present work was to examine the effects of VDD on the morphological, biomechanical and functional properties of cerebral arterioles., Methods: Four-week-old male Wistar rats (n = 11 per group) were either fed with vitamin D deficient diet or received conventional rat chow with per os vitamin D supplementation. Cardiovascular parameters and hormone levels (testosterone, androstenedione, progesterone and 25-hydroxyvitamin D) were measured during the study. After 8 weeks of treatment anterior cerebral artery segments were prepared and their morphological, biomechanical and functional properties were examined using pressure microangiometry. Resorcin-fuchsin and smooth muscle actin staining were used to detect elastic fiber density and smooth muscle cell counts in the vessel wall, respectively. Sections were immunostained for eNOS and COX-2 as well., Results: VDD markedly increased the wall thickness, the wall-to-lumen ratio and the wall cross-sectional area of arterioles as well as the number of smooth muscle cells in the tunica media. As a consequence, tangential wall stress was significantly lower in the VDD group. In addition, VDD increased the myogenic as well as the uridine 5'-triphosphate-induced tone and impaired bradykinin-induced relaxation. Decreased eNOS and increased COX-2 expression were also observed in the endothelium of VDD animals., Conclusions: VDD causes inward hypertrophic remodeling due to vascular smooth muscle cell proliferation and enhances the vessel tone probably because of increased vasoconstrictor prostanoid levels in young adult rats. In addition, the decreased eNOS expression results in endothelial dysfunction. These morphological and functional alterations can potentially compromise the cerebral circulation and lead to cerebrovascular disorders in VDD.

Tubal infertility and particularly, proximal tubal occlusion (15-25%) is gaining increasing attention among experts of reproductive medicine. In case of bilateral tubal occlusion in vitro fertilization is indicated, since the expected pregnancy rate is the same as can be expected from macrosurgical procedures. Despite the fact that better and better results are being obtained by sophisticated assisted reproduction techniques, in vitro fertilization procedures that are performed unnecessarily or not indicated objectively can result in serious consequences for the patients as well as for health insurance. Therefore, there is no question that refining procedures used for evaluating the tubal patency is extremely important in order to reduce physical and psychological burden on the patients, as well as from the viewpoint of cost-effectiveness. We demonstrate an optional protocol which can be performed as a one-step evaluation and recommend a diagnostic method to assure tubal patency. The procedure is easy to perform by diagnostic hysteroscopy, and according to our experience, the examination is highly accurate.

Based on the hypothesis that the predisposition to thrombosis in women suffering from deep venous thrombosis at young age can disturb also the uteroplacental circulation, the authors retrospectively analyzed the fetal outcome of 333 pregnancies in 101 women with thromboembolic event before 40 years of age and compared it to the fetal outcome of 2943 pregnancies in 1000 randomly selected obstetrical patients without thrombosis. The relative risks of adverse fetal outcomes in thromboembolic women were as follows: 1.85 (95% C.I.: 1.35-2.55) for the spontaneous miscarriage, 3.9 (95% C.I.: 2.20-6.93) for the second-trimester miscarriage, 1.74 (95% C.I.: 1.15-2.64) for the low birth weight, 2.82 (95% C.I.: 1.28-6.30) for the perinatal loss and 7.17 (95% C.I.: 2.64-19.47) for the abruption of placentae. Data obtained suggest that women with deep venous thrombosis at young age should encounter a higher risk of the uteroplacental thrombosis which results in increasing fetal morbidity and mortality during the second and third trimesters of gestation.