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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
2007-4-9
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pubmed:abstractText |
Elevated activities of the sympathetic nerve and renin-angiotensin systems are common features of heart failure. This study was designed to investigate the roles of the AT1 receptor in cardiac hypertrophy and oxidative stress during excessive beta-adrenoceptor stimulation using an AT1 receptor antagonist (ARB) and AT1a receptor-deficient (AT1aR(-/-)) mice. Isoproterenol (ISO) was given to C57BL mice with or without ARB (olmesartan) treatment and to AT1aR(-/-) mice by a subcutaneously implanted osmotic mini-pump for 11 days at a rate of 15 mg/kg/day. Chronic ISO infusion to C57BL mice caused concentric cardiac hypertrophy (sham; 4.1+/-0.1, ISO; 5.2+/-0.2 mg/g heart to body weight ratio), accompanied by enhancement of cardiac collagen accumulation, lipid peroxidation, superoxide generation and NADPH oxidase activity. The AT1a and beta-1,2 receptor mRNA expressions were down-regulated in the heart of ISO-infused mice. Olmesartan markedly suppressed cardiac mass enlargement as well as increases of oxidative indicators without any effects on heart rate. Olmesartan did not affect the cardiac angiotensin and beta-adrenergic receptor mRNA expression patterns. The AT1a receptor contribution to ISO-induced cardiac hypertrophy was reproduced in AT1aR(-/-) mice. These data suggest that the AT1 receptor plays a crucial role in the development of cardiac hypertrophy and oxidative stress under excessive beta-adrenergic stimulation, and that ARB treatment is beneficial for sympatho-excitatory cardiac hypertrophy and failure in mice.
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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/Adrenergic beta-Agonists,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensins,
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants,
http://linkedlifedata.com/resource/pubmed/chemical/Collagen Type I,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP Response...,
http://linkedlifedata.com/resource/pubmed/chemical/Isoproterenol,
http://linkedlifedata.com/resource/pubmed/chemical/NADPH Oxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, beta,
http://linkedlifedata.com/resource/pubmed/chemical/Superoxides
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0022-2828
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
42
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
804-11
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pubmed:meshHeading |
pubmed-meshheading:17350036-Adrenergic beta-Agonists,
pubmed-meshheading:17350036-Angiotensins,
pubmed-meshheading:17350036-Animals,
pubmed-meshheading:17350036-Antioxidants,
pubmed-meshheading:17350036-Blotting, Western,
pubmed-meshheading:17350036-Cardiomegaly,
pubmed-meshheading:17350036-Collagen Type I,
pubmed-meshheading:17350036-Cyclic AMP Response Element-Binding Protein,
pubmed-meshheading:17350036-Fibrosis,
pubmed-meshheading:17350036-Isoproterenol,
pubmed-meshheading:17350036-Lipid Peroxidation,
pubmed-meshheading:17350036-Male,
pubmed-meshheading:17350036-Mice,
pubmed-meshheading:17350036-Mice, Inbred C57BL,
pubmed-meshheading:17350036-Mice, Knockout,
pubmed-meshheading:17350036-Myocardium,
pubmed-meshheading:17350036-NADPH Oxidase,
pubmed-meshheading:17350036-Oxidative Stress,
pubmed-meshheading:17350036-Receptor, Angiotensin, Type 1,
pubmed-meshheading:17350036-Receptors, Adrenergic, beta,
pubmed-meshheading:17350036-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:17350036-Superoxides
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pubmed:year |
2007
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pubmed:articleTitle |
Role of AT1 receptor in isoproterenol-induced cardiac hypertrophy and oxidative stress in mice.
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pubmed:affiliation |
Department of Pharmacology, Kagawa University Medical School, 1750-1 Ikenobe, Miki, Kagawa 761-0793, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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