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B6D2F1 Mice Are a Suitable Model of Oxidative Stress–Mediated Impaired Endothelium-Dependent Dilation With Aging

By Lisa A. Lesniewski, Melanie L. Connell, Jessica R. Durrant, Brian J. Folian, Martin C. Anderson, Anthony J. Donato and Douglas R. Seals

Abstract

To determine if B6D2F1 mice represent a suitable model of oxidative stress–mediated impaired endothelium-dependent dilation (EDD) with aging, mice were studied at 6.9 ± 0.3 and 31.9 ± 0.6 months. EDD to acetylcholine (ACh) was 26% (p < .001) and 12% (p < .001) lower, respectively, in isolated carotid (n = 10–11) and femoral (n = 10) arteries from older mice, and reductions in arterial pressure to systemic ACh infusion were smaller in older mice (n = 6–10; p < .01). Nitrotyrosine was marked in aorta of older mice (p < .05, n = 4). Superoxide production in carotid arteries was greater (p < .05), and TEMPOL restored dilation in carotid arteries and systemically in older mice. NG-nitro-l-arginine methyl ester (l-NAME) reduced carotid artery dilation in young more than older mice, whereas TEMPOL restored the effects of l-NAME in older mice. Carotid artery stiffness was increased in older compared with young mice (p = .04). Our results provide the first comprehensive evidence that B6D2F1 mice are a useful model for investigating mechanisms of reduced nitric oxide–dependent, oxidative stress–associated EDD and increased arterial stiffness with aging

Topics: Articles
Publisher: Oxford University Press
OAI identifier: oai:pubmedcentral.nih.gov:2691198
Provided by: PubMed Central
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