阿托伐他汀可降低慢性肾脏病患者的交感神经活性。

Atorvastatin reduces sympathetic activity in patients with chronic kidney disease.

机构信息

Department of Nephrology and Hypertension, Rudolf Magnus Institute of Neuroscience, University Medical Center Utrecht, Utrecht, The Netherlands.

出版信息

J Hypertens. 2011 Nov;29(11):2176-80. doi: 10.1097/HJH.0b013e32834ae3c7.

DOI:10.1097/HJH.0b013e32834ae3c7

PMID:21897294

Abstract

BACKGROUND

Hypertensive chronic kidney disease (CKD) patients often have sympathetic hyperactivity, which appears to contribute to the pathogenesis of hypertension and cardiovascular organ damage. Experimental studies and some clinical studies have shown that statin therapy can reduce central sympathetic activity. Blockade of the renin-angiotensin system (RAS), which is standard treatment for CKD, is known to lower sympathetic activity. We hypothesized that adding a statin for 6 weeks to RAS blockade would further lower sympathetic activity in hypertensive stage 2-4 CKD patients.

METHODS

In 10 stable CKD patients (eight men, aged 45 ± 11 years, estimated glomerular filtration rate 56 ± 22 ml/min per 1.73 m2), who were on chronic treatment with aliskiren 300 mg, blood pressure and sympathetic activity (quantified by assessment of muscle sympathetic nerve activity, MSNA) were assessed at baseline and 6 weeks after atorvastatin 20 mg/day was added. Ten other CKD patients served as time control and were studied twice with an interval of 6 weeks without any change in medication, to quantify within participant reproducibility.

RESULTS

Mean arterial blood pressure remained stable throughout the study (93 ± 5 versus 94 ± 5 mmHg). MSNA was reduced from 28 ± 8 to 20 ± 6 bursts/min (P = 0.01), while heart rate remained stable during the study. In the control CKD group, MSNA did not change: 26 ± 5 to 25 ± 6 bursts/min. Atorvastatin reduced total and low-density lipoprotein cholesterol.

CONCLUSION

Atorvastatin has a further sympatholytic effect in CKD patients, who are on chronic aliskiren, which is independent of blood pressure and heart rate.

摘要

背景

高血压慢性肾脏病（CKD）患者常伴有交感神经活性亢进，这似乎是高血压和心血管器官损害的发病机制之一。实验研究和一些临床研究表明，他汀类药物治疗可以降低中枢交感神经活性。肾素-血管紧张素系统（RAS）阻断是 CKD 的标准治疗方法，已知其可以降低交感神经活性。我们假设，在 RAS 阻断的基础上加用他汀类药物治疗 6 周，可进一步降低高血压 2-4 期 CKD 患者的交感神经活性。

方法

在 10 例稳定的 CKD 患者（8 例男性，年龄 45 ± 11 岁，估计肾小球滤过率 56 ± 22 ml/min/1.73 m2）中，他们正在接受慢性阿利克仑 300 mg 治疗，在阿托伐他汀 20 mg/天治疗 6 周前后评估血压和交感神经活性（通过评估肌交感神经活动来量化，MSNA）。另外 10 例 CKD 患者作为时间对照，在没有任何药物变化的情况下，两次进行研究，间隔 6 周，以量化参与者内的可重复性。

结果

整个研究过程中平均动脉压保持稳定（93 ± 5 与 94 ± 5 mmHg）。MSNA 从 28 ± 8 降至 20 ± 6 爆发/分钟（P = 0.01），而心率在研究期间保持稳定。在对照组 CKD 患者中，MSNA 没有变化：26 ± 5 至 25 ± 6 爆发/分钟。阿托伐他汀降低了总胆固醇和低密度脂蛋白胆固醇。