Institute of Clinical Experimental Research, Semmelweis University, Faculty of Medicine, Budapest, Hungary.
Institute of Clinical Experimental Research, Semmelweis University, Faculty of Medicine, Budapest, Hungary.
Microvasc Res. 2019 Mar;122:78-84. doi: 10.1016/j.mvr.2018.11.011. Epub 2018 Nov 28.
Vitamin D (VitD) hypovitaminosis and androgen excess (AE) are both risk factors for cardiovascular diseases in fertile women. However, the possible early interaction between AE and VitD status is not clear. Our goal was to describe how VitD status influences early changes in the biomechanical reactivity of small coronary arterioles in adult female rats after transdermal testosterone treatment. Forty-six adolescent, 90-110-gram-weighed female Wistar rats were randomly grouped into 4 groups. Twenty-four animals received an optimal VitD-supplemented diet, from which 12 animals underwent transdermal testosterone treatment. Twenty-two animals received a VitD-deficient diet, from which 11 were treated with testosterone. At 8 weeks of treatment, invasive arterial blood pressure was registered after in vivo cannulation of carotid artery. Arteriolar end and side branches (200 μm diameter) of the left anterior descendent coronary artery (LAD) were obtained and examined with pressure arteriography in vitro. Similar segments were removed for histological examination. The inner and outer radii of the arterioles were measured using video-microscopy. Normal myogenic tone, maximal passive vasorelaxation and vasoconstriction of the arterioles were measured and statistically analyzed. The vessels' maximal smooth muscle relaxant potential, thromboxane-induced contraction capacity and normal myogenic tone were significantly influenced by actual VitD status. A lower relaxation capacity and increased wall thickness were observed in VitD-deficient groups, which could cause rigidity of the coronary arterioles and elevate cardiovascular risk. Supplementation of VitD could improve myogenic tone and relaxation and hold cardiovascular benefits.
维生素 D (VitD) 不足和雄激素过多 (AE) 都是生育期女性心血管疾病的危险因素。然而,AE 和 VitD 状态之间可能的早期相互作用尚不清楚。我们的目标是描述 VitD 状态如何影响经皮睾酮治疗后成年雌性大鼠小冠状动脉血管生物力学反应性的早期变化。46 只青春期、体重 90-110 克的雌性 Wistar 大鼠被随机分为 4 组。24 只动物接受了最佳 VitD 补充饮食,其中 12 只接受了经皮睾酮治疗。22 只动物接受了 VitD 缺乏饮食,其中 11 只接受了睾酮治疗。在 8 周的治疗后,通过颈总动脉的体内插管记录了有创动脉血压。获取并在体外通过压力血管造影术检查左前降支冠状动脉 (LAD) 的小动脉末端和侧支(200 μm 直径)。相似的节段被切除用于组织学检查。使用视频显微镜测量小动脉的内、外半径。测量并统计分析了小动脉的正常肌源性张力、最大被动血管舒张和血管收缩。血管的最大平滑肌松弛潜能、血栓烷诱导的收缩能力和正常肌源性张力受到实际 VitD 状态的显著影响。在 VitD 缺乏组中观察到舒张能力降低和壁厚度增加,这可能导致冠状动脉小动脉僵硬,并增加心血管风险。VitD 的补充可以改善肌源性张力和松弛度,并带来心血管益处。