| Thyroid hormone modulates the responsiveness of rat aorta to alpha1-adrenergic stimulation: an effect due to increased activation of beta2-adrenergic signaling. | |
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MedLine Citation:
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PMID: 20087285 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIM:The ability of the thyroid hormone to increase cardiac output and to lower systemic vascular resistance may provide a novel treatment for cardiovascular diseases. Therefore, understanding the mechanisms of thyroid hormone action on the heart and peripheral vasculature could be of clinical importance. We previously found that thyroid hormone modulates the alpha1-adrenergic effect on vascular reactivity of rat aortas. In the present study we further investigated possible mechanisms of this response. METHODS: Hyperthyroidism was induced on Wistar-Kyoto male rats with L-Thyroxine, (THYR) treatment for two weeks, N.=18 while untreated rats used as controls (NORM), N.=16. The thoracic aorta was dissected and cut into rings that were suspended in an isolated organ bath with Krebs-Henseleit buffer. Maximal tension, Tmax, in g was measured in response to Potassium Chloride (KCl) and Phenylephrine (PE) in rings in the presence of Ritodrine, a beta-2 agonist (NORM-RITO, N:=8, THYR-RITO, N.=9), or in the absence of Ritodrine (THYR, N.=9, NORM, N.=8). RESULTS: With KCL, Tmax was not different between the THYR, NORM, NORM-RITO, and THYR-RITO groups. With PE, there was a difference in Tmax between NORM-RITO and NORM, 0.66 (0.056) g vs 1.00 (0.066) g, P<0.05 and THYR and NORM, 0.75 (0.055) g vs 1.00 (0.066) g, P<0.05. No significant difference was observed between THYR-RITO AND THYR. Furthermore, Relax % was not significantly different between the NORM and the THYR, NORM-RITO, and THYR-RITO groups, 64.5%(3.7) vs 67.3%(6.7), 73.5% (4.3) and 81.8 %(4.7), P>0.05. CONCLUSIONS: PE induced vasoconstriction in isolated rat aortic rings was reduced after both ritodrine and thyroxine treatment. However, co-administration of thyroid hormone and ritodrine did not result in a synergistic reduction of PE induced vasoconstriction. Thus, thyroxine may modulate the alpha1-adrenergic vascular responsiveness by enhancing beta2-adrenergic stimulation. |
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Authors:
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M Pappas; K Mourouzis; H Karageorgiou; C Tesseromatis; I Mourouzis; G Kostopanagiotou; C Pantos; D V Cokkinos |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: International angiology : a journal of the International Union of Angiology Volume: 28 ISSN: 0392-9590 ISO Abbreviation: Int Angiol Publication Date: 2009 Dec |
Date Detail:
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Created Date: 2010-01-20 Completed Date: 2010-10-12 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8402693 Medline TA: Int Angiol Country: Italy |
Other Details:
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Languages: eng Pagination: 474-8 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, University of Athens, Athens, Greece. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Acetylcholine
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pharmacology Adrenergic alpha-Agonists / pharmacology Adrenergic beta-Agonists / pharmacology Animals Aorta, Thoracic / drug effects, metabolism*, physiopathology Disease Models, Animal Dose-Response Relationship, Drug Hyperthyroidism / metabolism*, physiopathology Male Phenylephrine / pharmacology Potassium Chloride / pharmacology Rats Rats, Inbred WKY Receptors, Adrenergic, alpha-1 / agonists, metabolism* Receptors, Adrenergic, beta-2 / agonists, metabolism* Ritodrine / pharmacology Signal Transduction* / drug effects Thyroxine / metabolism* Vasoconstriction* / drug effects Vasoconstrictor Agents / pharmacology Vasodilation Vasodilator Agents / pharmacology |
| Chemical | |
Reg. No./Substance:
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0/Adrenergic alpha-Agonists; 0/Adrenergic beta-Agonists; 0/Receptors, Adrenergic, alpha-1; 0/Receptors, Adrenergic, beta-2; 0/Vasoconstrictor Agents; 0/Vasodilator Agents; 26652-09-5/Ritodrine; 51-84-3/Acetylcholine; 59-42-7/Phenylephrine; 7447-40-7/Potassium Chloride; 7488-70-2/Thyroxine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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