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Heart Rate Contributes to the Vascular Effects of Chronic Mental Stress: Effects on Endothelial Function and Ischemic Brain Injury in Mice

F Custodis, K Gertz, M Balkaya, V Prinz, I Mathar... - Stroke, 2011 - Am Heart Assoc ISSN: 1524-4628 Copyright 2011 American Heart Association. All rights reserved. Print ISSN: 0039-2499. Online Stroke is published by the American Heart Association. 7272 Greenville Avenue, Dallas, TX 72514 DOI: 10.1161/STROKEAHA.110.598607 published online Apr ...

Results—Stress increased HR from 514±10 bpm to 570±14 bpm, this was prevented by ivabradine (485±7 bpm). Endothelium-dependent relaxation of aortic rings was impaired in mice exposed to stress. HR reduction restored endothelial function to the level of naive controls. Vascular lipid hydroperoxides were increased to 333%±24% and vascular NADPH oxidase activity was upregulated to 223±38% in stressed mice, which was prevented by ivabradine. Stress reduced aortic endothelial nitric oxide synthase m RNA expression to 84%±3% and increased AT1 receptor m RNA to 168%±18%. Both effects were attenuated by HR reduction. In brain tissue, stress resulted in an upregulation of lipid hydroperoxides to 140%±11%, which was attenuated by HR reduction. Ivabradine increased brain capillary density in naive and in stressed mice. Mice exposed to chronic stress before induction of ischemic stroke by transient middle cerebral artery occlusion exhibited increased lesion size (33.7±2.3 mm3 versus 23.9±2.4 mm3). HR reduction led to a marked reduction of the infarct volume to 12.9±3.3 mm3.