The effect of vitamin D on renin-angiotensin system activation and blood pressure: a randomized control trial.
The effect of vitamin D on renin-angiotensin system activation and blood pressure: a randomized control trial.
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DOI：
10.1097/hjh.0000000000001220
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发表时间：
2017-04
影响因子：
4.9
通讯作者：
Forman JP
中科院分区：
文献类型：
--
作者：
McMullan CJ;Borgi L;Curhan GC;Fisher N;Forman JP
啮齿类动物中维生素D信号传导的中断导致肾素血管紧张素系统（RAS）的激活和高血压的发展。对人类的观察性研究发现，较低的循环25-羟基维生素D（25 [OH] D）与RAS活性和血压（BP）升高相关。我们进行了第一个随机对照试验，以研究维生素D补充对人类RAS的影响。维生素D缺乏（25 [OH] D ≤ 20 ng/mL）、超重且无高血压的个体被随机分配到一项双盲、安慰剂对照试验中，接受麦角钙化醇或安慰剂治疗8周。在基线和第8周，采用高钠平衡状态下肾血浆流量（RPF）对卡托普利的反应测定肾脏特异性RAS活性，并评估全身RAS活性和24小时动态血压。84名参与者完成了研究。麦角钙化醇组的平均25 [OH] D水平从14.7 ng/mL增加到30.3 ng/mL，p值<0.0001，安慰剂组从14.3 ng/mL增加到17.4 ng/mL，p值= 0.3。麦角钙化醇组对卡托普利的RPF反应在基线时为33.9 ± 56.1 mL/min/1.73 m2，在第8周时为35.7 ± 47.7 mL/min/1.73 m2（p值= 0.83）;安慰剂组在基线时为37.3 ± 46.9 mL/min/1.73 m2，在第8周时为35.9 ± 26.2 mL/min/1.73 m2（p值= 0.78）。麦角钙化醇对PRA、AngII或24小时BP测量值无影响。这项试验发现，8周后纠正维生素D缺乏对RAS活性或血压没有好处。这些发现与维生素D是维生素D缺乏者降低血压的可改变目标的假设不一致。
Disruption of vitamin D signaling in rodents causes activation of the renin angiotensin system (RAS) and development of hypertension. Observational studies in humans found lower circulating 25-hydroxyvitamin D (25[OH]D) is associated with increased RAS activity and blood pressure (BP). We performed the first randomized control trial to investigate the effects of vitamin D supplementation on the RAS in humans. Vitamin D deficient, (25[OH]D ≤20 ng/mL), overweight individuals without hypertension were randomized into a double-blind, placebo-controlled trial of 8 weeks treatment with ergocalciferol or placebo. Kidney-specific RAS activity, measured using renal plasma flow (RPF) response to captopril in high sodium balance, was assessed at baseline and 8 weeks, as was systemic RAS activity and 24-hour ambulatory BP. 84 participants completed the study. Mean 25[OH]D levels increased from 14.7 to 30.3 ng/mL in the ergocalciferol group, p-value < 0.0001, and from 14.3 to 17.4 ng/mL in the placebo group, p-value = 0.3. The RPF response to captopril was 33.9±56.1 mL/min/1.73m2 at baseline and 35.7±47.7 mL/min/1.73m2 at 8 weeks in the ergocalciferol group (p-value=0.83); and was 37.3±46.9 mL/min/1.73m2 at baseline and 35.9±26.2 mL/min/1.73m2 at 8 weeks in the placebo group (p-value=0.78). Ergocalciferol had no effect on PRA, AngII, or 24-hour BP measurements. This trial found no benefit from correcting vitamin D deficiency on RAS activity or BP after 8 weeks. These findings are not consistent with the hypothesis that vitamin D is a modifiable target for lowering blood pressure in vitamin D deficient individuals.