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rdf:type |
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lifeskim:mentions |
umls-concept:C0003009,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0030685,
umls-concept:C0086418,
umls-concept:C0205263,
umls-concept:C0225336,
umls-concept:C0242606,
umls-concept:C0391871,
umls-concept:C0597357,
umls-concept:C0680242,
umls-concept:C0680255,
umls-concept:C1280500,
umls-concept:C1283071,
umls-concept:C1412113,
umls-concept:C1958507,
umls-concept:C1963578
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pubmed:issue |
7
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pubmed:dateCreated |
2008-10-15
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pubmed:abstractText |
Mechanical forces and the activation of the renin-angiotensin system (RAS) may alter the NO/O2(*-) balance, imparing endothelial nitric oxide (NO) availability. This study investigates the link between RAS and NO/O2(*-) balance in human aortic endothelial cells (HAEC) exposed to pulsatile stretch with and without ACE inhibitor quinaprilat or angiotensin II type 1 (AT(1)) receptor antagonist losartan. Pulsatile stretch increased Ang II levels and O2(*-) production, reducing NO release. RAS blockade with quinaprilat or losartan restored the balance between NO and O2(*-). These results provide a molecular basis for understanding the vascular protective effects of ACE inhibition and AT(1) receptor antagonism.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II Type 1 Receptor...,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin-Converting Enzyme...,
http://linkedlifedata.com/resource/pubmed/chemical/Losartan,
http://linkedlifedata.com/resource/pubmed/chemical/NOS3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type III,
http://linkedlifedata.com/resource/pubmed/chemical/Superoxides,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrahydroisoquinolines,
http://linkedlifedata.com/resource/pubmed/chemical/quinaprilat
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1525-6006
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
30
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
616-27
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pubmed:meshHeading |
pubmed-meshheading:18855265-Angiotensin II,
pubmed-meshheading:18855265-Angiotensin II Type 1 Receptor Blockers,
pubmed-meshheading:18855265-Angiotensin-Converting Enzyme Inhibitors,
pubmed-meshheading:18855265-Biomechanics,
pubmed-meshheading:18855265-Cells, Cultured,
pubmed-meshheading:18855265-Endothelial Cells,
pubmed-meshheading:18855265-Hemorheology,
pubmed-meshheading:18855265-Humans,
pubmed-meshheading:18855265-Losartan,
pubmed-meshheading:18855265-Models, Biological,
pubmed-meshheading:18855265-Nitric Oxide,
pubmed-meshheading:18855265-Nitric Oxide Synthase Type III,
pubmed-meshheading:18855265-Oxidative Stress,
pubmed-meshheading:18855265-Pulsatile Flow,
pubmed-meshheading:18855265-Renin-Angiotensin System,
pubmed-meshheading:18855265-Stress, Mechanical,
pubmed-meshheading:18855265-Superoxides,
pubmed-meshheading:18855265-Tetrahydroisoquinolines
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pubmed:year |
2008
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pubmed:articleTitle |
Pulsatile stretch induces release of angiotensin II and oxidative stress in human endothelial cells: effects of ACE inhibition and AT1 receptor antagonism.
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pubmed:affiliation |
Cardiovascular Center, University Hospital and Cardiovascular Research, Institute of Physiology, Zurich, Switzerland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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