Document Detail

Age and exercise training alter signaling through reactive oxygen species in the endothelium of skeletal muscle arterioles.
MedLine Citation:
PMID:  23288555     Owner:  NLM     Status:  MEDLINE    
Exercise training ameliorates age-related impairments in endothelium-dependent vasodilation in skeletal muscle arterioles. Additionally, exercise training is associated with increased superoxide production. The purpose of this study was to determine the role of superoxide and superoxide-derived reactive oxygen species (ROS) signaling in mediating endothelium-dependent vasodilation of soleus muscle resistance arterioles from young and old, sedentary and exercise-trained rats. Young (3 mo) and old (22 mo) male rats were either exercise trained or remained sedentary for 10 wk. To determine the impact of ROS signaling on endothelium-dependent vasodilation, responses to acetylcholine were studied under control conditions and during the scavenging of superoxide and/or hydrogen peroxide. To determine the impact of NADPH oxidase-derived ROS, endothelium-dependent vasodilation was determined following NADPH oxidase inhibition. Reactivity to superoxide and hydrogen peroxide was also determined. Tempol, a scavenger of superoxide, and inhibitors of NADPH oxidase reduced endothelium-dependent vasodilation in all groups. Similarly, treatment with catalase and simultaneous treatment with tempol and catalase reduced endothelium-dependent vasodilation in all groups. Decomposition of peroxynitrite also reduced endothelium-dependent vasodilation. Aging had no effect on arteriolar protein content of SOD-1, catalase, or glutathione peroxidase-1; however, exercise training increased protein content of SOD-1 in young and old rats, catalase in young rats, and glutathione peroxidase-1 in old rats. These data indicate that ROS signaling is necessary for endothelium-dependent vasodilation in soleus muscle arterioles, and that exercise training-induced enhancement of endothelial function occurs, in part, through an increase in ROS signaling.
Amy L Sindler; Rafael Reyes; Bei Chen; Payal Ghosh; Alvaro N Gurovich; Lori S Kang; Arturo J Cardounel; Michael D Delp; Judy M Muller-Delp
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2013-01-03
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  114     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2013 Mar 
Date Detail:
Created Date:  2013-03-04     Completed Date:  2014-01-13     Revised Date:  2014-03-07    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  681-93     Citation Subset:  IM    
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MeSH Terms
Acetylcholine / pharmacology
Age Factors
Arterioles / drug effects,  metabolism,  physiology
Catalase / metabolism
Cyclic N-Oxides / metabolism
Endothelium, Vascular / drug effects,  metabolism*,  physiology
Endothelium-Dependent Relaxing Factors / pharmacology
Glutathione Peroxidase / metabolism
Hydrogen Peroxide / metabolism
Muscle, Skeletal / blood supply*,  drug effects,  metabolism*,  physiology
NADPH Oxidase / metabolism
Nitric Oxide / metabolism
Physical Conditioning, Animal / physiology*
Random Allocation
Rats, Inbred F344
Reactive Oxygen Species / metabolism*
Signal Transduction / drug effects,  physiology*
Spin Labels
Superoxides / metabolism
Vascular Resistance
Vasodilation / drug effects,  physiology
Grant Support
Reg. No./Substance:
0/Cyclic N-Oxides; 0/Endothelium-Dependent Relaxing Factors; 0/Reactive Oxygen Species; 0/Spin Labels; 11062-77-4/Superoxides; 2226-96-2/tempol; 31C4KY9ESH/Nitric Oxide; BBX060AN9V/Hydrogen Peroxide; EC 1.11.1.-/glutathione peroxidase GPX1; EC; EC Peroxidase; EC Oxidase; N9YNS0M02X/Acetylcholine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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