焦虑诱导的血浆去甲肾上腺素增加会增强原发性高血压患者单核细胞的活性氧生成。

Anxiety-induced plasma norepinephrine augmentation increases reactive oxygen species formation by monocytes in essential hypertension.

作者信息

Yasunari Kenichi, Matsui Tokuzo, Maeda Kensaku, Nakamura Munehiro, Watanabe Takanori, Kiriike Nobuo

机构信息

Department of General Medicine and Cardiology, Graduate School of Medicine, Osaka City University, Osaka 545-8585, Japan.

出版信息

Am J Hypertens. 2006 Jun;19(6):573-8. doi: 10.1016/j.amjhyper.2005.10.027.

DOI:10.1016/j.amjhyper.2005.10.027

PMID:16733228

Abstract

BACKGROUND

An association between anxiety and depression and increased blood pressure (BP) and cardiovascular disease risk has not been firmly established. We examined the hypothesis that anxiety and depression lead to increased plasma catecholamines and to production of reactive oxygen species (ROS) by mononuclear cells (MNC) in hypertensive individuals. We also studied the role of BP in this effect.

METHODS

In Protocol 1, a cross-sectional study was performed in 146 hypertensive patients to evaluate whether anxiety and depression affect BP and ROS formation by MNC through increasing plasma catecholamines. In Protocol 2, a 6-month randomized controlled trial using a subtherapeutic dose of the alpha(1)-adrenergic receptor antagonist doxazosin (1 mg/day) versus placebo in 86 patients with essential hypertension was performed to determine whether the increase in ROS formation by MNC was independent of BP.

RESULTS

In Protocol 1, a significant relationship was observed between the following: trait anxiety and plasma norepinephrine (r = 0.32, P < .01); plasma norepinephrine and ROS formation by MNC (r = 0.36, P < .01); and plasma norepinephrine and systolic, diastolic, and mean BP (r = 0.17, P = .04; r = 0.26, P = .02; r = 0.23, P < .01, respectively). In Protocol 2, subtherapeutic doxazosin treatment (1 mg/day) had no significant effect on BP. However doxazosin significantly decreased ROS formation by MNC compared with placebo (P < .01).

CONCLUSION

Trait anxiety may increase plasma norepinephrine and increase ROS formation by MNC independent of BP in hypertensive patients.

摘要

背景

焦虑和抑郁与血压升高及心血管疾病风险之间的关联尚未完全确立。我们检验了以下假设：焦虑和抑郁会导致高血压个体血浆儿茶酚胺增加以及单核细胞（MNC）产生活性氧（ROS）。我们还研究了血压在这一效应中的作用。

方法

在方案1中，对146例高血压患者进行了一项横断面研究，以评估焦虑和抑郁是否通过增加血浆儿茶酚胺来影响血压和MNC产生ROS。在方案2中，对86例原发性高血压患者进行了一项为期6个月的随机对照试验，使用亚治疗剂量的α1肾上腺素能受体拮抗剂多沙唑嗪（1毫克/天）与安慰剂进行对比，以确定MNC产生ROS的增加是否独立于血压。

结果

在方案1中，观察到以下各项之间存在显著关系：特质焦虑与血浆去甲肾上腺素（r = 0.32，P < 0.01）；血浆去甲肾上腺素与MNC产生ROS（r = 0.36，P < 0.01）；以及血浆去甲肾上腺素与收缩压、舒张压和平均血压（分别为r = 0.17，P = 0.04；r = 0.26，P = 0.02；r = 0.23，P < 0.01）。在方案2中，亚治疗剂量的多沙唑嗪治疗（1毫克/天）对血压无显著影响。然而，与安慰剂相比，多沙唑嗪显著降低了MNC产生ROS的水平（P < 0.01）。