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慢性应激和罗格列酮会增加雄性大鼠的血管僵硬度指标。

Chronic stress and Rosiglitazone increase indices of vascular stiffness in male rats.

作者信息

Goodson M L, Packard A E B, Buesing D R, Maney M, Myers B, Fang Y, Basford J E, Hui D Y, Ulrich-Lai Y M, Herman J P, Ryan Karen K

机构信息

Department of Neurobiology, Physiology, and Behavior, College of Biological Sciences, University of California, Davis, CA, United States.

Department of Psychiatry and Behavioral Neuroscience, University of Cincinnati College of Medicine, Cincinnati, OH, United States.

出版信息

Physiol Behav. 2017 Apr 1;172:16-23. doi: 10.1016/j.physbeh.2016.03.031. Epub 2016 Mar 31.

Abstract

Prolonged and/or frequent exposure to psychological stress responses may lead to deterioration of organs and tissues, predisposing to disease. In agreement with this, chronic psychosocial stress is linked to greater cardiovascular risk, including increased incidence of atherosclerosis, myocardial ischemia, coronary heart disease, and death. Thus the association between stress and cardiovascular dysfunction represents an important node for therapeutic intervention in cardiovascular disease. Here we report that 2weeks of chronic variable stress (CVS) increased indices of vascular stiffness, including increased collagen deposition in the aortic adventitia and increased resting pulse pressure, in male rats. Thus CVS may represent a useful rodent model for stress-associated CVD, especially for aging populations for which widening pulse pressure is a well-known risk factor. Additionally, we report that the thiazolidinedione Rosiglitazone (RSG) blunts chronic stress-associated increases in circulating corticosterone. Despite this, RSG was not protective against adverse cardiovascular outcomes associated with chronic stress. Rather RSG itself is associated with increased pulse pressure, and this is exacerbated by chronic stress-highlighting that chronic stress may represent an additional contributor to RSG-associated cardiovascular risk.

摘要

长期和/或频繁暴露于心理应激反应可能导致器官和组织的恶化,易患疾病。与此一致的是,慢性心理社会应激与更高的心血管风险相关,包括动脉粥样硬化、心肌缺血、冠心病和死亡的发生率增加。因此,应激与心血管功能障碍之间的关联是心血管疾病治疗干预的一个重要节点。在此我们报告,在雄性大鼠中,2周的慢性可变应激(CVS)增加了血管僵硬度指标,包括主动脉外膜胶原沉积增加和静息脉压升高。因此,CVS可能是一种用于应激相关心血管疾病的有用啮齿动物模型,特别是对于脉压增宽是一个众所周知的危险因素的老年人群。此外,我们报告噻唑烷二酮类药物罗格列酮(RSG)可减弱慢性应激相关的循环皮质酮增加。尽管如此,RSG对与慢性应激相关的不良心血管结局并无保护作用。相反,RSG本身与脉压增加有关,并且慢性应激会加剧这种情况——这突出表明慢性应激可能是RSG相关心血管风险的另一个促成因素。

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