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25-羟维生素 D 状态、动脉僵硬度与健康人体中的肾素-血管紧张素系统。

25-Hydroxyvitamin D status, arterial stiffness and the renin-angiotensin system in healthy humans.

机构信息

Department of Medicine, University of Calgary , Calgary, AB , Canada and.

出版信息

Clin Exp Hypertens. 2014;36(6):386-91. doi: 10.3109/10641963.2013.827705. Epub 2013 Oct 28.

DOI:10.3109/10641963.2013.827705
PMID:24164282
Abstract

Vitamin D deficiency is associated with increased arterial stiffness. We sought to clarify the influence of vitamin D in modulating angiotensin II-dependent arterial stiffness. Thirty-six healthy subjects (33 ± 2 years, 67% female, mean 25-hydroxyvitamin D 69 ± 4 nmol/L) were studied in high salt balance. Arterial stiffness, expressed as brachial pulse wave velocity (bPWV) and aortic augmentation index (AIx), was measured by tonometry at baseline and in response to angiotensin II infusion (3 ng/kg/min × 30 min then 6 ng/kg/min × 30 min). The primary outcome was change in bPWV after an angiotensin II challenge. Results were analyzed according to plasma 25-hydroxyvitamin D status: deficient (<50 nmol/L) and sufficient (≥ 50 nmol/L). There were no differences in baseline arterial stiffness between vitamin D deficient (25-hydroxyvitamin D 40 ± 2 nmol/L) and sufficient (25-hydroxyvitamin D 80 ± 4 nmol/L) groups. Compared with sufficient vitamin D status, vitamin D deficiency was associated with a decreased arterial response to angiotensin II challenge (Δbrachial pulse wave velocity: 0.48 ± 0.44 m/s versus 1.95 ± 0.22 m/s, p=0.004; Δaortic augmentation index: 9.4 ± 3.4% versus 14.2 ± 2.7%, p=0.3), which persisted for brachial pulse wave velocity response after adjustment for covariates (p=0.03). Vitamin D deficiency is associated with increased arterial stiffness in healthy humans, possibly through an angiotensin II-dependent mechanism.

摘要

维生素 D 缺乏与动脉僵硬度增加有关。我们旨在阐明维生素 D 对血管紧张素 II 依赖性动脉僵硬度的调节作用。36 名健康受试者(33±2 岁,67%为女性,平均 25-羟维生素 D 69±4 nmol/L)在高盐平衡状态下接受研究。通过动脉张力测定法,在基线和血管紧张素 II 输注(3ng/kg/min×30min 然后 6ng/kg/min×30min)时测量动脉僵硬度,以肱动脉脉搏波速度(bPWV)和主动脉增强指数(AIx)表示。主要终点为血管紧张素 II 挑战后 bPWV 的变化。根据血浆 25-羟维生素 D 状态对结果进行分析:不足(<50nmol/L)和充足(≥50nmol/L)。维生素 D 不足(25-羟维生素 D 40±2nmol/L)和充足(25-羟维生素 D 80±4nmol/L)组之间的基础动脉僵硬度无差异。与充足的维生素 D 状态相比,维生素 D 缺乏与对血管紧张素 II 挑战的动脉反应降低有关(肱动脉脉搏波速度变化:0.48±0.44m/s 与 1.95±0.22m/s,p=0.004;主动脉增强指数变化:9.4±3.4%与 14.2±2.7%,p=0.3),在调整协变量后,这种差异仍然存在于 bPWV 反应中(p=0.03)。维生素 D 缺乏与健康人群的动脉僵硬度增加有关,这可能是通过血管紧张素 II 依赖性机制。

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