| Effect of AT1 receptor blockade on intermittent hypoxia-induced endothelial dysfunction. | |
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MedLine Citation:
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PMID: 22728949 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Noah J Marcus; Nathan R Philippi; Cynthia E Bird; Yu-Long Li; Harold D Schultz; Barbara J Morgan |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2012-06-21 |
Journal Detail:
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Title: Respiratory physiology & neurobiology Volume: 183 ISSN: 1878-1519 ISO Abbreviation: Respir Physiol Neurobiol Publication Date: 2012 Aug |
Date Detail:
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Created Date: 2012-07-31 Completed Date: 2013-01-04 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 101140022 Medline TA: Respir Physiol Neurobiol Country: Netherlands |
Other Details:
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Languages: eng Pagination: 67-74 Citation Subset: IM |
Copyright Information:
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Copyright © 2012 Elsevier B.V. All rights reserved. |
Affiliation:
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John Rankin Laboratory of Pulmonary Medicine, University of Wisconsin, Madison, WI 53706-1532, USA. nmarcus@unmc.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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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:
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HL 074072/HL/NHLBI NIH HHS; T32 HL07654/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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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 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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