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rdf:type |
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lifeskim:mentions |
umls-concept:C0020564,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0026844,
umls-concept:C0032578,
umls-concept:C0205191,
umls-concept:C0225828,
umls-concept:C0678226,
umls-concept:C1135918,
umls-concept:C1515655,
umls-concept:C1518425
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pubmed:issue |
1 Pt 2
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pubmed:dateCreated |
1998-2-23
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pubmed:abstractText |
To assess the vascular and cardiac response to NO (nitric oxide) synthase (NOS) blockade in vivo, Wistar-Kyoto rats (WKY) were treated for 3 wk with NG-nitro-L-arginine methyl ester (L-NAME; 10 mg.kg-1.day-1). L-NAME treatment induced hypertension that was associated with increased plasma renin activity. Flow cytometry cell cycle DNA analysis showed that aortic vascular smooth muscle cells (VSMC) from L-NAME-treated WKY had a significantly higher polyploid population compared with WKY controls. Using organ bath experiments, we have shown that aortic rings from L-NAME-treated WKY have an increased contractile response to phenylephrine and impaired relaxation to carbachol compared with control rings. NOS blockade in vivo caused a significant increase in cardiac and left ventricular hypertrophy. Northern mRNA analysis of the myocardium showed that L-NAME treatment caused reexpression of the fetal skeletal alpha-actin isoform without alterations in collagen type I expression, a pattern indicating true hypertrophy of the cardiomyocytes. These studies provide further insight to confirm that NO deficiency in vivo results in the development of vascular and cardiac hypertrophy.
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0002-9513
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
274
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H52-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:9458851-Actins,
pubmed-meshheading:9458851-Aldosterone,
pubmed-meshheading:9458851-Animals,
pubmed-meshheading:9458851-Aorta, Thoracic,
pubmed-meshheading:9458851-Carbachol,
pubmed-meshheading:9458851-Cardiomegaly,
pubmed-meshheading:9458851-Cell Cycle,
pubmed-meshheading:9458851-DNA,
pubmed-meshheading:9458851-Heart,
pubmed-meshheading:9458851-Hypertension,
pubmed-meshheading:9458851-Isometric Contraction,
pubmed-meshheading:9458851-Muscle, Skeletal,
pubmed-meshheading:9458851-Muscle, Smooth, Vascular,
pubmed-meshheading:9458851-Myocardium,
pubmed-meshheading:9458851-NG-Nitroarginine Methyl Ester,
pubmed-meshheading:9458851-Nitric Oxide Synthase,
pubmed-meshheading:9458851-Nitroprusside,
pubmed-meshheading:9458851-Phenylephrine,
pubmed-meshheading:9458851-Polyploidy,
pubmed-meshheading:9458851-RNA, Messenger,
pubmed-meshheading:9458851-Rats,
pubmed-meshheading:9458851-Rats, Inbred WKY,
pubmed-meshheading:9458851-Renin-Angiotensin System,
pubmed-meshheading:9458851-Transcription, Genetic
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pubmed:year |
1998
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pubmed:articleTitle |
Vascular smooth muscle cell polyploidy and cardiomyocyte hypertrophy due to chronic NOS inhibition in vivo.
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pubmed:affiliation |
Department of Medicine and Therapeutics, University of Glasgow, Western Infirmary, United Kingdom.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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