pubmed-article:9277473 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9277473 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:9277473 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:9277473 | lifeskim:mentions | umls-concept:C0020550 | lld:lifeskim |
pubmed-article:9277473 | lifeskim:mentions | umls-concept:C0035096 | lld:lifeskim |
pubmed-article:9277473 | lifeskim:mentions | umls-concept:C1383860 | lld:lifeskim |
pubmed-article:9277473 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:9277473 | pubmed:issue | 2 Pt 2 | lld:pubmed |
pubmed-article:9277473 | pubmed:dateCreated | 1997-9-25 | lld:pubmed |
pubmed-article:9277473 | pubmed:abstractText | This study was conducted to examine whether the renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy without involving the sympathetic nervous system. Sprague-Dawley rats were divided into control-innervated, control-denervated, hyperthyroid-innervated, and hyperthyroid-denervated groups using intraperitoneal injections of thyroxine and 6-hydroxydopamine. After 8 wk, the heart-to-body weight ratio increased in hyperthyroid groups (63%), and this increase was only partially inhibited by sympathetic denervation. Radioimmunoassays and reverse transcription-polymerase chain reaction revealed increased cardiac levels of renin (33%) and angiotensin II (53%) and enhanced cardiac expression of renin mRNA (225%) in the hyperthyroid groups. These increases were unaffected by sympathetic denervation or 24-h bilateral nephrectomy. In addition, losartan and nicardipine decreased systolic blood pressure to the same extent, but only losartan caused regression of thyroxine-induced cardiac hypertrophy. These results suggest that thyroid hormone activates the cardiac renin-angiotensin system without involving the sympathetic nervous system or the circulating renin-angiotensin system; the activated renin-angiotensin system contributes to cardiac hypertrophy in hyperthyroidism. | lld:pubmed |
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pubmed-article:9277473 | pubmed:language | eng | lld:pubmed |
pubmed-article:9277473 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9277473 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:9277473 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:9277473 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9277473 | pubmed:month | Aug | lld:pubmed |
pubmed-article:9277473 | pubmed:issn | 0002-9513 | lld:pubmed |
pubmed-article:9277473 | pubmed:author | pubmed-author:SuzukiHH | lld:pubmed |
pubmed-article:9277473 | pubmed:author | pubmed-author:MiyashitaYY | lld:pubmed |
pubmed-article:9277473 | pubmed:author | pubmed-author:IchiharaAA | lld:pubmed |
pubmed-article:9277473 | pubmed:author | pubmed-author:HayashiMM | lld:pubmed |
pubmed-article:9277473 | pubmed:author | pubmed-author:TakenakaTT | lld:pubmed |
pubmed-article:9277473 | pubmed:author | pubmed-author:SarutaTT | lld:pubmed |
pubmed-article:9277473 | pubmed:author | pubmed-author:KoboriHH | lld:pubmed |
pubmed-article:9277473 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9277473 | pubmed:volume | 273 | lld:pubmed |
pubmed-article:9277473 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9277473 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9277473 | pubmed:pagination | H593-9 | lld:pubmed |
pubmed-article:9277473 | pubmed:dateRevised | 2010-8-13 | lld:pubmed |
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pubmed-article:9277473 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9277473 | pubmed:articleTitle | Role of the renin-angiotensin system in cardiac hypertrophy induced in rats by hyperthyroidism. | lld:pubmed |
pubmed-article:9277473 | pubmed:affiliation | Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan. | lld:pubmed |
pubmed-article:9277473 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9277473 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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