Vitamin D Deficiency-induced Hypertension Is Associated With Vascular Oxidative Stress and Altered Heart Gene Expression
Vitamin D Deficiency-induced Hypertension Is Associated With Vascular Oxidative Stress and Altered Heart Gene Expression
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DOI：
10.1097/fjc.0b013e31821c832f
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发表时间：
2011-07-01
影响因子：
3
通讯作者：
Moreno-Reyes, Rodrigo
中科院分区：
文献类型：
--
作者：
Argacha, Jean-Francois;Egrise, Dominique;Moreno-Reyes, Rodrigo
维生素 D 缺乏 (VDD) 与心血管风险增加有关。我们研究了 VDD 对喂食缺乏维生素 D 的饮食的生长中雄性大鼠心血管系统的影响。使用离体的大鼠主动脉，我们评估了超氧阴离子和内皮依赖性舒张。微阵列技术用于识别 VDD 引起的心脏基因表达的变化。与对照组相比，VDD增加了收缩压（P < 0.05）和主动脉壁中超氧阴离子的产生（P < 0.05），并且倾向于增加血管紧张素II和心房钠尿肽的血清水平（P < 0.15）。然而，VDD 对乙酰胆碱的最大松弛度略有改善，从 75% +/- 3% 到 83% +/- 2% (P < 0.05)。用硝基-L-精氨酸甲酯 (L-NAME) 或过氧化氢酶孵育主动脉环并不能消除在缺乏维生素 D 的大鼠中观察到的内皮介导的舒张增强作用。只有与吲哚美辛或钙激活钾通道阻滞剂一起孵育才能抑制这种差异。与对照相比，51个基因的表达呈现出不同的表达，其中包括多个参与氧化应激和心肌肥厚调节的基因。总之，生命早期的 VDD 会增加动脉血压，促进血管氧化应激，并诱导心脏基因表达的变化。然而，内皮介导的血管舒缩张力调节在不依赖于NO的代偿途径的整个增强过程中得以维持。
Vitamin D deficiency (VDD) is associated with an increased cardiovascular risk. We investigated the effect of VDD on the cardiovascular system of growing male rats fed with a vitamin D-deficient diet. Using isolated rat aorta, we assessed both superoxide anion and endothelial-dependent relaxations. Microarray technology was used to identify changes induced by VDD in cardiac gene expression. Compared with control, VDD increased systolic blood pressure (P < 0.05) and superoxide anion production in the aortic wall (P < 0.05) and tended to increase serum levels of angiotensin II and atrial natriuretic peptide (P < 0.15). However, VDD slightly improved maximal relaxation to acetylcholine from 75% +/- 3% to 83% +/- 2% (P < 0.05). Incubation of aortic rings either with nitro-L-arginine methyl ester (L-NAME) or catalase did not eliminate the enhancement of endothelial-mediated relaxation observed in vitamin D-deficient rats. Only incubation with indometacin or calcium-activated potassium channels blockers suppressed this difference. Compared with control, the expression of 51 genes showed different expression, including several genes involved in the regulation of oxidative stress and myocardial hypertrophy. In conclusion, VDD in early life increases arterial blood pressure, promotes vascular oxidative stress, and induces changes in cardiac gene expression. However, the endothelial-mediated regulation of vasomotor tone is maintained throughout the enhancement of an NO-independent compensatory pathway.