Zaheer Sarah, Taquechel Kiara, Brown Jenifer M, Adler Gail K, Williams Jonathan S, Vaidya Anand
1 Division of Endocrinology, Diabetes, and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, USA.
2 Northeastern University, USA.
J Renin Angiotensin Aldosterone Syst. 2018 Jan-Mar;19(1):1470320317754178. doi: 10.1177/1470320317754178.
Prior studies suggest that vitamin D therapy may decrease cardiovascular disease risk in type 2 diabetes (T2DM) by lowering renin-angiotensin system (RAS) activity. However, randomized human intervention studies to evaluate the effect of vitamin D receptor (VDR) agonists on RAS activity are lacking.
The objective of this article is to investigate the effect of direct VDR activation with calcitriol on circulating RAS activity and vascular hemodynamics in T2DM.
A randomized, double-blinded, and placebo-controlled study wherein 18 participants with well-controlled T2DM without chronic kidney disease (CKD) were administered calcitriol or placebo for three weeks was conducted. Outcome measures included plasma renin activity (PRA), serum and urinary aldosterone, mean arterial pressure (MAP) before and after an infusion of angiotensin II, and renal plasma flow (RPF) via para-aminohippurate clearance.
Despite an increase in 1,25(OH)D with calcitriol administration (45.4 to 61.8 pg/ml, p = 0.03) and no change with placebo, there were no significant differences in PRA, serum or urinary aldosterone, baseline and angiotensin II-stimulated MAP, or basal and angiotensin II-stimulated RPF between interventions.
In this randomized and placebo-controlled study in participants with T2DM without CKD, calcitriol therapy to raise 1,25(OH)D levels, when compared with placebo, did not significantly change circulating RAS activity or vascular hemodynamics.
先前的研究表明，维生素D疗法可能通过降低肾素-血管紧张素系统（RAS）活性来降低2型糖尿病（T2DM）患者的心血管疾病风险。然而，缺乏评估维生素D受体（VDR）激动剂对RAS活性影响的随机人体干预研究。
本文旨在研究骨化三醇直接激活VDR对T2DM患者循环RAS活性和血管血流动力学的影响。
进行了一项随机、双盲、安慰剂对照研究，18名T2DM控制良好且无慢性肾脏病（CKD）的参与者被给予骨化三醇或安慰剂，为期三周。观察指标包括血浆肾素活性（PRA）、血清和尿醛固酮、输注血管紧张素II前后的平均动脉压（MAP）以及通过对氨基马尿酸清除率测定的肾血浆流量（RPF）。
尽管给予骨化三醇后1,25(OH)D升高（从45.4至61.8 pg/ml，p = 0.03），而安慰剂组无变化，但干预组之间在PRA、血清或尿醛固酮、基线和血管紧张素II刺激后的MAP，或基础和血管紧张素II刺激后的RPF方面均无显著差异。
在这项针对无CKD的T2DM参与者的随机安慰剂对照研究中，与安慰剂相比，骨化三醇疗法提高1,25(OH)D水平并未显著改变循环RAS活性或血管血流动力学。
