| pubmed-article:17350036 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17350036 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:17350036 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:17350036 | lifeskim:mentions | umls-concept:C0242606 | lld:lifeskim |
| pubmed-article:17350036 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:17350036 | lifeskim:mentions | umls-concept:C1383860 | lld:lifeskim |
| pubmed-article:17350036 | lifeskim:mentions | umls-concept:C1412113 | lld:lifeskim |
| pubmed-article:17350036 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:17350036 | pubmed:dateCreated | 2007-4-9 | lld:pubmed |
| pubmed-article:17350036 | 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. | lld:pubmed |
| pubmed-article:17350036 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17350036 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17350036 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17350036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17350036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17350036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17350036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17350036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17350036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17350036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17350036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17350036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17350036 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17350036 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17350036 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:17350036 | pubmed:issn | 0022-2828 | lld:pubmed |
| pubmed-article:17350036 | pubmed:author | pubmed-author:NishiyamaAkir... | lld:pubmed |
| pubmed-article:17350036 | pubmed:author | pubmed-author:KimuraShojiS | lld:pubmed |
| pubmed-article:17350036 | pubmed:author | pubmed-author:AbeYouichiY | lld:pubmed |
| pubmed-article:17350036 | pubmed:author | pubmed-author:FujisawaYoshi... | lld:pubmed |
| pubmed-article:17350036 | pubmed:author | pubmed-author:OhmoriKojiK | lld:pubmed |
| pubmed-article:17350036 | pubmed:author | pubmed-author:NagaiYukikoY | lld:pubmed |
| pubmed-article:17350036 | pubmed:author | pubmed-author:ZhangGuo-Xing... | lld:pubmed |
| pubmed-article:17350036 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17350036 | pubmed:volume | 42 | lld:pubmed |
| pubmed-article:17350036 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17350036 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17350036 | pubmed:pagination | 804-11 | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:meshHeading | pubmed-meshheading:17350036... | lld:pubmed |
| pubmed-article:17350036 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17350036 | pubmed:articleTitle | Role of AT1 receptor in isoproterenol-induced cardiac hypertrophy and oxidative stress in mice. | lld:pubmed |
| pubmed-article:17350036 | pubmed:affiliation | Department of Pharmacology, Kagawa University Medical School, 1750-1 Ikenobe, Miki, Kagawa 761-0793, Japan. | lld:pubmed |
| pubmed-article:17350036 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17350036 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:11607 | entrezgene:pubmed | pubmed-article:17350036 | lld:entrezgene |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17350036 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17350036 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17350036 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17350036 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17350036 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:17350036 | lld:pubmed |
