Arteriolar biomechanics in a rat polycystic ovary syndrome model - effects of parallel vitamin D3 treatment.

To clarify the effects of dihydrotestosterone (DHT)-induced polycystic ovary syndrome (PCOS) on arteriolar biomechanics in a rat model and the possible modulatory role of vitamin D3. METHODS AND RESULTS: The PCOS model was induced in female Wistar rats by ten-weeks DHT treatment. Arteriolar biomechanics was tested in arterioles by pressure arteriography in control as well as DHT- and DHT with vitamin D3-treated animals in contracted and passive conditions. Increased wall stress and distensibility as well as increased vascular lumen were detected after DHT treatment. Concomitant vitamin D3 treatment lowered the mechanical load of the arterioles and restored the vascular diameter. CONCLUSION: The hyperandrogenic state resulted in more rigid, less flexible arteriolar walls with increased vascular lumen compared with controls. DHT treatment caused eutrophic remodelling of gracilis arteriole. These prehypertensive alterations caused by chronic DHT treatment were mostly reversed by concomitant vitamin D3 administration

Effects of vitamin D3 derivative--calcitriol on pharmacological reactivity of aortic rings in a rodent PCOS model.

Abstract BACKGROUND: The aim of this study was to examine the effects of the hyperandrogenic state in dihydrotestosterone (DHT)-induced polycystic ovary syndrome (PCOS), the vascular responses to different vasoactive agents, and the modulatory role of vitamin D3. METHODS: APCOS model was induced by DHT application in 20 female Wistar rats. Ten of the DHT treated rats simultaneously received calcitriol treatment. After 10 weeks, myographs were used to test the reactivity of isolated thoracic aortic rings to norepinephrine and acetylcholine. Thereafter, the vascular rings were incubated with the NO-synthase blocker (nitro-L-arginine methyl ester) or the cyclooxygenase inhibitor (indomethacin) for 20 min, and the effects of norepinephrine and acetylcholine were re-evaluated. RESULTS: Norepinephrine-induced vasoconstriction was enhanced after DHT treatment, but this effect was attenuated by calcitriol administration. Vasorelaxation of DHT-treated thoracic aortic rings was impaired, but this could be partly reversed by calcitriol application. Impaired NO-dependent vasorelaxation in DHT-treated animals was mostly reversed by concomitant calcitriol administration, but this effect was diminished by prostanoid-dependent vasoconstriction. CONCLUSIONS: These studies show that the enhanced sensitivity to vasoconstrictors and impaired NO-dependent vasorelaxation in hyperandrogenic PCOS rats could be partially reversed by calcitriol treatment

Quantitative Analysis of Vasodilatory Action of Quercetin on Intramural Coronary Resistance Arteries of the Rat In Vitro

Background: Dietary quercetin improves cardiovascular health, relaxes some vascular smooth muscle and has been demonstrated to serve as a substrate for the cyclooxygenase enzyme. Aims: 1. To test quantitatively a potential direct vasodilatory effect on intramural coronary resistance artery segments, in different concentrations. 2. To scale vasorelaxation at different intraluminal pressure loads on such vessels of different size. 3. To test the potential role of prostanoids in vasodilatation induced by quercetin. Methods: Coronary arterioles (70-240 mu m) were prepared from 24 rats and pressurized in PSS, using a pressure microangiometer. Results: The spontaneous tone that developed at 50 mmHg was relaxed by quercetin in the 10(-9) moles/lit concentration (p<0.05), while 10(-5) moles/lit caused full relaxation. Significant relaxation was observed at all pressure levels (10-100 mmHg) at 10(-7) moles/lit concentration of quercetin. The cyclooxygenase blocker indomethacin (10(-5) moles/lit) induced no relaxation but contraction when physiological concentrations of quercetin were present in the tissue bath (p<0.02 with Anova), this contraction being more prominent in smaller vessels and in the higher pressure range (p<0.05, Pearson correlation). A further 2-8% contraction could be elicited by the NO blocker L-NAME (10(-4) moles/lit). Conclusion: These results demonstrate that circulating levels of quercetin (10(-7) moles/lit) exhibit a substantial coronary vasodilatory effect. The extent of it is commeasurable with that of several other physiological mechanisms of coronary blood flow control. At least part of this relaxation is the result of an altered balance toward the production of endogenous vasodilatory prostanoids in the coronary arteriole wall

From Living in Saltwater to a Scarcity of Salt and Water, and Then an Overabundance of Salt—The Biological Roller Coaster to Which the Renin–Angiotensin System Has Had to Adapt: An Editorial

Angiotensin II (Ang II) is a hormone with much more complex actions than is typical for other agonists with heterotrimeric G protein-coupled receptors (GPCRs) [...

Effect of indomethacin on inner diameter of quercetin-treated coronary arteriole segments.

<p>Note contraction with indomethacin (p<0.05 with ANOVA), in contrast the expected vasodilation, indicating the presence of vasodilatory prostanoids with the polyphenol. Indomethacin concentration was 10⁻⁵ moles/lit, represented by full circles, quercetin was in 10⁻⁷ moles/lit concentration, represented by empty circles.</p

Concentration-response curve of quercetin on coronary resistance arterioles of rat.

<p>Intramural coronary arteriole segments were spontaneously contracted, then dilatated by quercetin at intraluminal pressure 50 mmHg. (PSS, Krebs-Ringer solution, Ca²⁺-free, Ca²⁺-free solution). #, significantly different from fully relaxed; ¤, different from spontaneously contracted with ANOVA; * different from spontaneously contracted with the paired t-test.</p

Quercetin induced dilatation as function of morphological lumen size.

<p>We found no correlation (p>0.05 with Pearson's correlation).</p

Quercetin dilation on spontaneously contracted small coronary arterioles at different pressures.

<p>Full circles represents diameters in PSS, empty circles are diameters in quercetin 10⁻⁷ moles/lit. * p<0.05 with ANOVA</p

Vasoconstriction induced by L-NAME in coronary arteriole segments pretreated with quercetin and indomethacin.

<p>Concentrations: L-NAME: 10⁻⁴ moles/lit, quercetin: 10⁻⁷ moles/lit, and indomethacin: 10⁻⁵ moles/lit. * p<0.05 with ANOVA</p