Department of Nephrology and Hypertension, University of Erlangen-Nuremberg, Ulmenweg 18, 91054 Erlangen, Germany.
Clin Res Cardiol. 2013 Apr;102(4):299-304. doi: 10.1007/s00392-012-0534-1. Epub 2012 Dec 21.
Vitamin D deficiency is nowadays considered as a potential cardiovascular and renal risk factor. We tested the hypotheses that vitamin D deficiency impairs the endothelial function of renal vasculature and whether vitamin D levels and endothelial function can be improved by the treatment with statins.
In a double-blind, randomized study of 31 hypercholesterolemic patients with vitamin D insufficiency (<30 ng/ml) were randomly assigned to rosuvastatin (10 mg/d) and placebo for 6 weeks. Basal nitric oxide (NO) activity of the renal vasculature was assessed both before and after the blockade of NO synthases with systemic infusion of N(G)-monomethyl-L-arginine (L-NMMA). In parallel, 25(OH)D was measured.
Multiple regression analysis revealed that at baseline 25(OH)D is an independent determinant of basal NO activity as assessed by the decrease in RPF, in response to L-NMMA (β = -0.446, r = 0.015). Compared to placebo treatment, rosuvastatin increased 25(OH)D levels (21.6 ± 4.0 vs. 24.1 ± 8.1 ng/ml, p = 0.039). Basal NO activity was significantly more increased after 6-week therapy with rosuvastatin than with placebo (-94.8 ± 70 vs. -68.2 ± 32 ml/min, p = 0.044), indicating increased basal NOS activity after 6 weeks of rosuvastatin treatment. Basal NO activity in the placebo phase was correlated inversely with 25(OH)D (r = -0.385; p = 0.027).
Thus, vitamin D insufficiency is associated with impaired endothelial function in the renal vasculature and both were beneficially influenced by the treatment with rosuvastatin.
如今,维生素 D 缺乏被认为是心血管和肾脏的潜在风险因素。我们检验了以下假设:维生素 D 缺乏会损害肾血管的内皮功能,以及他汀类药物治疗是否可以提高维生素 D 水平和内皮功能。
在一项针对 31 名维生素 D 不足(<30ng/ml)的高胆固醇血症患者的双盲、随机研究中,患者被随机分为瑞舒伐他汀(10mg/d)和安慰剂组,治疗 6 周。在全身输注 N(G)-单甲基-L-精氨酸(L-NMMA)阻断一氧化氮合酶前后,评估肾血管的基础一氧化氮(NO)活性。同时,测量 25(OH)D。
多元回归分析显示,在基线时,25(OH)D 是基础 NO 活性的独立决定因素,其通过 L-NMMA 引起的 RPF 下降来评估(β=-0.446,r=0.015)。与安慰剂治疗相比,瑞舒伐他汀增加了 25(OH)D 水平(21.6±4.0 vs. 24.1±8.1ng/ml,p=0.039)。与安慰剂组相比,瑞舒伐他汀治疗 6 周后,基础 NO 活性显著增加(-94.8±70 vs. -68.2±32ml/min,p=0.044),表明瑞舒伐他汀治疗 6 周后基础 NOS 活性增加。安慰剂阶段的基础 NO 活性与 25(OH)D 呈负相关(r=-0.385;p=0.027)。
因此,维生素 D 不足与肾血管内皮功能受损有关,而这两者均受益于瑞舒伐他汀的治疗。