Document Detail


Differential effects of eNOS uncoupling on conduit and small arteries in GTP-cyclohydrolase I-deficient hph-1 mice.
MedLine Citation:
PMID:  21963838     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In the present study, we used the hph-1 mouse, which displays GTP-cyclohydrolase I (GTPCH I) deficiency, to test the hypothesis that loss of tetrahydrobiopterin (BH(4)) in conduit and small arteries activates compensatory mechanisms designed to protect vascular wall from oxidative stress induced by uncoupling of endothelial nitric oxide synthase (eNOS). Both GTPCH I activity and BH(4) levels were reduced in the aortas and small mesenteric arteries of hph-1 mice. However, the BH(4)-to-7,8-dihydrobiopterin ratio was significantly reduced only in hph-1 aortas. Furthermore, superoxide anion and 3-nitrotyrosine production were significantly enhanced in aortas but not in small mesenteric arteries of hph-1 mice. In contrast to the aorta, protein expression of copper- and zinc-containing superoxide dismutase (CuZnSOD) was significantly increased in small mesenteric arteries of hph-1 mice. Protein expression of catalase was increased in both aortas and small mesenteric arteries of hph-1 mice. Further analysis of endothelial nitric oxide synthase (eNOS)/cyclic guanosine monophosphate (cGMP) signaling demonstrated that protein expression of phosphorylated Ser(1177)-eNOS as well as basal cGMP levels and hydrogen peroxide was increased in hph-1 aortas. Increased production of hydrogen peroxide in hph-1 mice aortas appears to be the most likely mechanism responsible for phosphorylation of eNOS and elevation of cGMP. In contrast, upregulation of CuZnSOD and catalase in resistance arteries is sufficient to protect vascular tissue from increased production of reactive oxygen species generated by uncoupling of eNOS. The results of our study suggest that anatomical origin determines the ability of vessel wall to cope with oxidative stress induced by uncoupling of eNOS.
Authors:
Livius V d'Uscio; Leslie A Smith; Zvonimir S Katusic
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-09-30
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  301     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2011 Dec 
Date Detail:
Created Date:  2011-12-06     Completed Date:  2012-01-23     Revised Date:  2013-05-23    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H2227-34     Citation Subset:  IM    
Affiliation:
Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antioxidants / metabolism
Aorta / enzymology*
Biopterin / analogs & derivatives*,  deficiency,  metabolism
Catalase / metabolism
Cyclic GMP / metabolism
GTP Cyclohydrolase / deficiency*,  genetics
Hydrogen Peroxide / metabolism
Male
Mesenteric Arteries / enzymology*
Mice
Mice, Inbred C57BL
Mice, Knockout
Nitric Oxide Synthase Type III / metabolism*
Oxidative Stress
Phosphorylation
Serine
Superoxide Dismutase / metabolism
Superoxides / metabolism
Tyrosine / analogs & derivatives,  metabolism
Grant Support
ID/Acronym/Agency:
HL-53524/HL/NHLBI NIH HHS; HL-91867/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 11062-77-4/Superoxides; 17528-72-2/5,6,7,8-tetrahydrobiopterin; 22150-76-1/Biopterin; 3604-79-3/3-nitrotyrosine; 55520-40-6/Tyrosine; 56-45-1/Serine; 6779-87-9/7,8-dihydrobiopterin; 7665-99-8/Cyclic GMP; 7722-84-1/Hydrogen Peroxide; EC 1.11.1.6/Catalase; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, mouse; EC 1.15.1.1/Superoxide Dismutase; EC 3.5.4.16/GTP Cyclohydrolase
Comments/Corrections

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