pubmed-article:10362681 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10362681 | lifeskim:mentions | umls-concept:C0330390 | lld:lifeskim |
pubmed-article:10362681 | lifeskim:mentions | umls-concept:C0007226 | lld:lifeskim |
pubmed-article:10362681 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:10362681 | lifeskim:mentions | umls-concept:C0040135 | lld:lifeskim |
pubmed-article:10362681 | lifeskim:mentions | umls-concept:C0031437 | lld:lifeskim |
pubmed-article:10362681 | lifeskim:mentions | umls-concept:C0039476 | lld:lifeskim |
pubmed-article:10362681 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
pubmed-article:10362681 | lifeskim:mentions | umls-concept:C1879647 | lld:lifeskim |
pubmed-article:10362681 | pubmed:issue | 6 Pt 2 | lld:pubmed |
pubmed-article:10362681 | pubmed:dateCreated | 1999-7-22 | lld:pubmed |
pubmed-article:10362681 | pubmed:abstractText | We have used a telemetry system to record heart rate, body temperature, electrocardiogram (ECG), and locomotor activity in awake, freely moving mice lacking thyroid hormone receptor (TR)-beta or TR-alpha1 and -beta (TR-alpha1/beta). The TR-alpha1/beta-deficient mice had a reduced heart rate compared with wild-type controls. The TR-beta-deficient mice showed an elevated heart rate, which, however, was unresponsive to thyroid hormone treatment regardless of hormonal serum levels. ECG revealed that the TR-beta-deficient mice had a shortened Q-Tend time in contrast to the TR-alpha1/beta-deficient mice, which exhibited prolonged P-Q and Q-Tend times. Mental or pharmacological stimulation of the sympathetic nervous system resulted in a parallel increase in heart rate in all animals. A single injection of a nonselective beta-adrenergic-receptor blocker resulted in a parallel decrease in all mice. The TR-alpha1/beta-deficient mice also had a 0.4 degrees C lower body temperature than controls, whereas no difference was observed in locomotor activity between the different strains of mice. Our present and previous results support the hypothesis that TR-alpha1 has a major role in determining heart rate under baseline conditions and body temperature and that TR-beta mediates a hormone-induced increase in heart rate. | lld:pubmed |
pubmed-article:10362681 | pubmed:language | eng | lld:pubmed |
pubmed-article:10362681 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10362681 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:10362681 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10362681 | pubmed:month | Jun | lld:pubmed |
pubmed-article:10362681 | pubmed:issn | 0002-9513 | lld:pubmed |
pubmed-article:10362681 | pubmed:author | pubmed-author:ThorénPP | lld:pubmed |
pubmed-article:10362681 | pubmed:author | pubmed-author:JohanssonCC | lld:pubmed |
pubmed-article:10362681 | pubmed:author | pubmed-author:VennströmBB | lld:pubmed |
pubmed-article:10362681 | pubmed:author | pubmed-author:ForrestDD | lld:pubmed |
pubmed-article:10362681 | pubmed:author | pubmed-author:GötheSS | lld:pubmed |
pubmed-article:10362681 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10362681 | pubmed:volume | 276 | lld:pubmed |
pubmed-article:10362681 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10362681 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10362681 | pubmed:pagination | H2006-12 | lld:pubmed |
pubmed-article:10362681 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:10362681 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10362681 | pubmed:articleTitle | Cardiovascular phenotype and temperature control in mice lacking thyroid hormone receptor-beta or both alpha1 and beta. | lld:pubmed |
pubmed-article:10362681 | pubmed:affiliation | Department of Physiology and Pharmacology, Karolinska Institute, S-171 77 Stockholm, Sweden. Catarina.Johnansson@fyfa.ki.se | lld:pubmed |
pubmed-article:10362681 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10362681 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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