Document Detail

Interaction between endothelial heme oxygenase-2 and endothelin-1 in altered aortic reactivity after hypoxia in rats.
MedLine Citation:
PMID:  15486027     Owner:  NLM     Status:  MEDLINE    
The aim of this study was to determine whether increased expression of heme oxygenase (HO) contributes to impairment of aortic contractile responses after hypoxia through effects on reactivity to endothelin-1 (ET-1). Thoracic aortas from normoxic rats and rats exposed to hypoxia (10% O2) for 16 or 48 h were mounted in organ bath myographs for contractile studies, fixed in paraformaldehyde, or frozen in liquid nitrogen for protein extraction. In rings from normoxic rats, the HO inhibitor tin protoporphyrin IX (SnPP IX, 10 microM) did not alter the response to phenylephrine or ET-1. In rings from rats exposed to 16-h hypoxia, maximum tension generated in response to these agonists was higher in endothelium-intact but not -denuded rings in the presence of SnPP IX. In rings from rats exposed to 48-h hypoxia SnPP IX increased contraction in endothelium-intact but not -denuded rings. In endothelium-intact aortic rings from rats exposed to 16-h hypoxia incubated with endothelin A receptor-specific antagonist BQ-123 (10(-7) M), SnPP IX did not alter phenylephrine-induced contraction. Aortic ET-1 protein levels, measured by radioimmunoassay, were increased in rats exposed to hypoxia for 16 and 48 h. Western blotting showed that HO-1 and HO-2 protein were increased after 16 h of hypoxia and returned to near-control levels after 48 h. Increase in HO-1 protein was detected in endothelium-intact and -denuded rings. Removal of endothelium abolished the increase in HO-2 immunoreactivity. Immunohistochemistry localized expression of HO-1 protein to vascular smooth muscle, whereas HO-2 was only detected in endothelium. HO-2 is expressed by aortic endothelial cells early during hypoxic exposure and impairs ET-1-mediated potentiation of contraction to alpha-adrenoceptor stimulation.
Vasanthi Govindaraju; Hwee Teoh; Qutayba Hamid; Peter Cernacek; Michael E Ward
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2004-10-14
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  288     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2005 Feb 
Date Detail:
Created Date:  2005-01-14     Completed Date:  2005-02-23     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H962-70     Citation Subset:  IM    
Meakins Christie Laboratories, McGill University, Montreal, Quebec, Canada.
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MeSH Terms
Anoxia / metabolism*
Aorta, Thoracic / enzymology*
Endothelin-1 / metabolism*
Endothelium, Vascular / enzymology*
Enzyme Inhibitors / pharmacology
Heme Oxygenase (Decyclizing) / antagonists & inhibitors,  metabolism*
Heme Oxygenase-1
Metalloporphyrins / pharmacology
NG-Nitroarginine Methyl Ester / pharmacology
Oxygen / metabolism
Phenylephrine / pharmacology
Protoporphyrins / pharmacology
Rats, Sprague-Dawley
Vasoconstrictor Agents / pharmacology
Reg. No./Substance:
0/Endothelin-1; 0/Enzyme Inhibitors; 0/Metalloporphyrins; 0/Protoporphyrins; 0/Vasoconstrictor Agents; 14325-05-4/tin protoporphyrin IX; 50903-99-6/NG-Nitroarginine Methyl Ester; 59-42-7/Phenylephrine; 7782-44-7/Oxygen; EC Oxygenase (Decyclizing); EC Oxygenase-1; EC oxygenase-2

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

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