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. 2012 Aug 2;44(10):594–602. doi: 10.3858/emm.2012.44.10.068

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Copyright © 2012 by the Korean Society for Biochemistry and Molecular Biology

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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siArgII improved impaired vascular reactivity in aged mice. (A) Aged aortic vessels had augmented contractile responses to U46619 compared to young mice (^*, young vs. aged, P < 0.01). siArgII restored the U46619-mediated pressor response of aged aortic vessels to levels similar to that of young aortas (^*, young vs. aged, P < 0.01; ^**, aged vs. aged + siArgII, P < 0.01). n = 4 mice per each group. (B) siArgII attenuated contractile responses to U46619 in young aorta (^*, young vs. young + siArgII, P < 0.01) and ABH incubation with old aorta significantly retarded U46619-dependent constriction (^**, aged vs. aged + ABH, P < 0.01). (C) Endothelium-dependent relaxation responses to Ach were impaired in aged aortas (^*, young vs. aged, P < 0.01). Impaired relaxation was recovered with siArgII pretreatment (^**, aged vs. aged + siArgII, P < 0.05). n = 4 mice per each group. (D) ABH incubation augmented Ach-dependent vessel relaxation in aged aorta (^*, aged vs. aged + ABH, P < 0.01).