Document Detail


Sustained activation of AMPK ameliorates age-associated vascular endothelial dysfunction via a nitric oxide-independent mechanism.
MedLine Citation:
PMID:  22484146     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Exercise restores endothelium-dependent dilation (EDD) in old mice by reducing oxidative stress and increasing nitric oxide (NO) bioavailability. Adenosine monophosphate protein kinase (AMPK) activation mimics some effects of exercise. Old (28-30 months) B6D2F1 mice had reduced arterial AMPK expression and superoxide-mediated suppression of EDD vs. young (3-6 months) controls. Pharmacological activation of AMPK by aminoimidazole carboxamide ribonucleotide (AICAR) for 2 weeks increased arterial AMPK and reversed this superoxide-induced impairment of EDD. The improvement in EDD was independent of NO or prostaglandin signaling, suggesting enhanced endothelium-dependent hyperpolarizing factor-related dilation. AMPK activation may represent a novel therapy for treating age-associated vascular dysfunction.
Authors:
Lisa A Lesniewski; Melanie C Zigler; Jessica R Durrant; Anthony J Donato; Douglas R Seals
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-03-28
Journal Detail:
Title:  Mechanisms of ageing and development     Volume:  133     ISSN:  1872-6216     ISO Abbreviation:  Mech. Ageing Dev.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-05-23     Completed Date:  2012-10-01     Revised Date:  2014-03-19    
Medline Journal Info:
Nlm Unique ID:  0347227     Medline TA:  Mech Ageing Dev     Country:  Ireland    
Other Details:
Languages:  eng     Pagination:  368-71     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
AMP-Activated Protein Kinases / metabolism*
Aging / drug effects,  metabolism*
Aminoimidazole Carboxamide / analogs & derivatives,  pharmacology
Animals
Antioxidants / pharmacology
Cyclic N-Oxides / pharmacology
Endothelium, Vascular / drug effects,  enzymology*
Mice
Nitric Oxide / metabolism
Ribonucleotides / pharmacology
Signal Transduction / drug effects,  physiology
Spin Labels
Superoxides / antagonists & inhibitors,  metabolism
Vasodilation / drug effects,  physiology
Vasodilator Agents / pharmacology
Grant Support
ID/Acronym/Agency:
AG000279/AG/NIA NIH HHS; AG013038/AG/NIA NIH HHS; AG029337/AG/NIA NIH HHS; AG033196/AG/NIA NIH HHS; AG033755/AG/NIA NIH HHS; AG040297/AG/NIA NIH HHS; HL107120/HL/NHLBI NIH HHS; K01 AG029337/AG/NIA NIH HHS; K01 AG033196/AG/NIA NIH HHS; R01 AG040297/AG/NIA NIH HHS; R01 HL107120/HL/NHLBI NIH HHS; R21 AG033755/AG/NIA NIH HHS; R37 AG013038/AG/NIA NIH HHS; T32 AG000279/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Cyclic N-Oxides; 0/Ribonucleotides; 0/Spin Labels; 0/Vasodilator Agents; 11062-77-4/Superoxides; 2226-96-2/tempol; 31C4KY9ESH/Nitric Oxide; 360-97-4/Aminoimidazole Carboxamide; EC 2.7.11.1/AMP-Activated Protein Kinases; F0X88YW0YK/AICA ribonucleotide
Comments/Corrections

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