Document Detail


Coronary endothelial function and vascular smooth muscle proliferation are programmed by early-gestation dexamethasone exposure in sheep.
MedLine Citation:
PMID:  20335378     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Exposure of the early-gestation ovine fetus to exogenous glucocorticoids induces changes in postnatal cardiovascular physiology. We sought to characterize coronary artery vascular function in this model by elucidating the contribution of nitric oxide and reactive oxygen species to altered coronary vascular reactivity and examining the proliferative potential of coronary artery vascular smooth muscle cells. Dexamethasone (dex, 0.28 mg x kg(-1) x day(-1) for 48 h) was administered to pregnant ewes at 27-28-day gestation (term 145 days). Coronary arteries were isolated from 1- to 2-wk-old dex-exposed offspring and aged-matched controls. Compared with controls, coronary arteries from dex-exposed lambs demonstrated enhanced vasoconstriction to endothelin-1 and ACh that was abolished by endothelial removal or preincubation with the nitric oxide synthase inhibitor L-NNA, membrane-permeable superoxide dismutase + catalase, or apamin + charybdotoxin, but not indomethacin. The rate of coronary vascular smooth muscle cell (VSMC) proliferation was also significantly greater in dex-exposed lambs. Protein levels of the proliferating cell nuclear antigen were increased and alpha-smooth muscle actin decreased in dex-exposed coronary VSMC, consistent with a proliferative state. Finally, expression of the NADPH oxidase Nox 4, but not Nox 1, mRNA was also decreased in coronary VSMC from dex-exposed lambs. These findings suggest an important interaction exists between early-gestation glucocorticoid exposure and reactive oxygen species that is associated with alterations in endothelial function and coronary VSMC proliferation. These changes in coronary physiology are consistent with those associated with the development of atherosclerosis and may provide an important link between an adverse intrauterine environment and increased risk for coronary artery disease.
Authors:
Kenneth A Volk; Robert D Roghair; Felicia Jung; Thomas D Scholz; Fred S Lamb; Jeffrey L Segar
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-03-24
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  298     ISSN:  1522-1490     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-25     Completed Date:  2010-06-15     Revised Date:  2011-07-28    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R1607-14     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, University of Iowa, Iowa City, Iowa 52242, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Catalase / metabolism
Coronary Vessels / metabolism
Dexamethasone / pharmacology*
Endothelin-1 / pharmacology
Endothelium / metabolism*
Female
Fetus / metabolism
Glucocorticoids / pharmacology*
Muscle, Smooth, Vascular / metabolism*
Nitric Oxide / metabolism
Nitric Oxide Synthase Type III
Pregnancy
Sheep / metabolism*
Superoxide Dismutase / metabolism
Vasoconstriction / drug effects
Grant Support
ID/Acronym/Agency:
ES 012268/ES/NIEHS NIH HHS; HD 050359/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Endothelin-1; 0/Glucocorticoids; 10102-43-9/Nitric Oxide; 50-02-2/Dexamethasone; EC 1.11.1.6/Catalase; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.15.1.1/Superoxide Dismutase
Comments/Corrections

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