| pubmed-article:12224825 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12224825 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
| pubmed-article:12224825 | lifeskim:mentions | umls-concept:C0022245 | lld:lifeskim |
| pubmed-article:12224825 | lifeskim:mentions | umls-concept:C0907532 | lld:lifeskim |
| pubmed-article:12224825 | lifeskim:mentions | umls-concept:C1383860 | lld:lifeskim |
| pubmed-article:12224825 | lifeskim:mentions | umls-concept:C0574032 | lld:lifeskim |
| pubmed-article:12224825 | lifeskim:mentions | umls-concept:C0599946 | lld:lifeskim |
| pubmed-article:12224825 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:12224825 | lifeskim:mentions | umls-concept:C0205191 | lld:lifeskim |
| pubmed-article:12224825 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:12224825 | pubmed:dateCreated | 2002-9-12 | lld:pubmed |
| pubmed-article:12224825 | pubmed:abstractText | Endogenous nitric oxide (NO) inhibits the contractile response to beta-adrenergic stimulation, but its effect on cardiac hypertrophy mediated by beta-adrenoceptors remains unclear. The present study was designed to determine whether overproduction of endothelial NO synthase (eNOS) could inhibit cardiac hypertrophy induced by chronic isoproterenol (ISO) infusion (30mg/kg per day) using eNOS overexpressing (eNOS-Tg) mice and wild-type (WT) mice. In a separate group, WT mice were treated with ISO and hydralazine to decrease blood pressure to the same levels in eNOS-Tg mice. The eNOS expression, NOS activity, and cGMP levels in the heart were remarkably higher in eNOS-Tg mice than in WT mice. ISO increased both heart weight and the heart/body weight ratio, which were significantly attenuated in eNOS-Tg mice compared with WT or hydralazine-treated WT mice. Histological examination revealed that the extent of fibrosis was not significantly different among the 3 groups, and that the increase in myocyte size was more than 10% lower in eNOS-Tg than in the other groups. In addition, up-regulated expression of atrial natriuretic peptide mRNA associated with cardiac hypertrophy was significantly inhibited in eNOS-Tg mice during ISO infusion. These results indicate that endogenous NO might act as a negative modulator for the hypertrophic response to beta-adrenergic stimulation. | lld:pubmed |
| pubmed-article:12224825 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12224825 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12224825 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12224825 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12224825 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12224825 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12224825 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12224825 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:12224825 | pubmed:issn | 1346-9843 | lld:pubmed |
| pubmed-article:12224825 | pubmed:author | pubmed-author:YokoyamaMitsu... | lld:pubmed |
| pubmed-article:12224825 | pubmed:author | pubmed-author:InoueNobutaka... | lld:pubmed |
| pubmed-article:12224825 | pubmed:author | pubmed-author:HirataKen-ich... | lld:pubmed |
| pubmed-article:12224825 | pubmed:author | pubmed-author:KawashimaSein... | lld:pubmed |
| pubmed-article:12224825 | pubmed:author | pubmed-author:OzakiMasanori... | lld:pubmed |
| pubmed-article:12224825 | pubmed:author | pubmed-author:YamashitaTomo... | lld:pubmed |
| pubmed-article:12224825 | pubmed:author | pubmed-author:HiraseTetsuak... | lld:pubmed |
| pubmed-article:12224825 | pubmed:author | pubmed-author:OhashiYoshita... | lld:pubmed |
| pubmed-article:12224825 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12224825 | pubmed:volume | 66 | lld:pubmed |
| pubmed-article:12224825 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12224825 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12224825 | pubmed:pagination | 851-6 | lld:pubmed |
| pubmed-article:12224825 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:12224825 | pubmed:meshHeading | pubmed-meshheading:12224825... | lld:pubmed |
| pubmed-article:12224825 | pubmed:meshHeading | pubmed-meshheading:12224825... | lld:pubmed |
| pubmed-article:12224825 | pubmed:meshHeading | pubmed-meshheading:12224825... | lld:pubmed |
| pubmed-article:12224825 | pubmed:meshHeading | pubmed-meshheading:12224825... | lld:pubmed |
| pubmed-article:12224825 | pubmed:meshHeading | pubmed-meshheading:12224825... | lld:pubmed |
| pubmed-article:12224825 | pubmed:meshHeading | pubmed-meshheading:12224825... | lld:pubmed |
| pubmed-article:12224825 | pubmed:meshHeading | pubmed-meshheading:12224825... | lld:pubmed |
| pubmed-article:12224825 | pubmed:meshHeading | pubmed-meshheading:12224825... | lld:pubmed |
| pubmed-article:12224825 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12224825 | pubmed:articleTitle | Overexpression of endothelial nitric oxide synthase attenuates cardiac hypertrophy induced by chronic isoproterenol infusion. | lld:pubmed |
| pubmed-article:12224825 | pubmed:affiliation | Department of Internal Medicine, Kobe University Graduate School of Medicine, Japan. | lld:pubmed |
| pubmed-article:12224825 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12224825 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:12224825 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:12224825 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:12224825 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:12224825 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:12224825 | lld:pubmed |
