Document Detail


Effect of AT1 receptor blockade on intermittent hypoxia-induced endothelial dysfunction.
MedLine Citation:
PMID:  22728949     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chronic intermittent hypoxia (CIH) raises arterial pressure, impairs vasodilator responsiveness, and increases circulating angiotensin II (Ang II); however, the role of Ang II in CIH-induced vascular dysfunction is unknown. Rats were exposed to CIH or room air (NORM), and a subset of these animals was treated with losartan (Los) during the exposure period. After 28 days, vasodilatory responses to acetylcholine or nitroprusside were measured in isolated gracilis arteries. Superoxide levels and Ang II receptor protein expression were measured in saphenous arteries. After 28 days, arterial pressure was increased and acetylcholine-induced vasodilation was blunted in CIH vs. NORM, and this was prevented by Los. Responses to nitroprusside and superoxide levels did not differ between CIH and NORM. Expression of AT(2)R was decreased and the AT(1)R:AT(2)R ratio was increased in CIH vs. NORM, but this was unaffected by Los. These results indicate that the blood pressure elevation and endothelial dysfunction associated with CIH is dependent, at least in part, on RAS signaling.
Authors:
Noah J Marcus; Nathan R Philippi; Cynthia E Bird; Yu-Long Li; Harold D Schultz; Barbara J Morgan
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-06-21
Journal Detail:
Title:  Respiratory physiology & neurobiology     Volume:  183     ISSN:  1878-1519     ISO Abbreviation:  Respir Physiol Neurobiol     Publication Date:  2012 Aug 
Date Detail:
Created Date:  2012-07-31     Completed Date:  2013-01-04     Revised Date:  2013-08-19    
Medline Journal Info:
Nlm Unique ID:  101140022     Medline TA:  Respir Physiol Neurobiol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  67-74     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier B.V. All rights reserved.
Affiliation:
John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin, Madison, WI 53706-1532, USA. nmarcus@unmc.edu
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / pharmacology
Angiotensin II Type 1 Receptor Blockers / pharmacology*
Animals
Anoxia / physiopathology*
Arteries / drug effects,  physiopathology
Endothelium, Vascular / drug effects,  physiopathology*
Losartan / pharmacology
Male
Nitroprusside / pharmacology
Rats
Rats, Sprague-Dawley
Receptor, Angiotensin, Type 1 / physiology*
Receptors, Angiotensin / biosynthesis
Signal Transduction / drug effects,  physiology
Superoxides / analysis
Vascular Resistance / drug effects,  physiology
Vasodilation / drug effects,  physiology
Grant Support
ID/Acronym/Agency:
HL 074072/HL/NHLBI NIH HHS; R01 HL074072/HL/NHLBI NIH HHS; T32 HL07654/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Angiotensin II Type 1 Receptor Blockers; 0/Receptor, Angiotensin, Type 1; 0/Receptors, Angiotensin; 11062-77-4/Superoxides; 114798-26-4/Losartan; 15078-28-1/Nitroprusside; 51-84-3/Acetylcholine
Comments/Corrections

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


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