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Article: Thyroid hormone affects both endothelial and vascular smooth muscle cells in rat arteries

TitleThyroid hormone affects both endothelial and vascular smooth muscle cells in rat arteries
Authors
Issue Date2015
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar
Citation
European Journal of Pharmacology, 2015, v. 747, p. 18-28 How to Cite?
AbstractHypothyroidism impairs endothelium-dependent dilatations, while hyperthyroidism augments the production of endothelial nitric oxide. Thus, experiments were designed to determine if thyroid hormone causes endothelium-dependent responses, or alleviates diabetic endothelial dysfunction. Isometric tension was measured in rings with or without endothelium of arteries from normal and diabetic Sprague-Dawley rats. Release of 6-keto prostaglandin F1α and thromboxane B2 were measured by enzyme linked immunosorbent assay and protein levels [endothelial nitric oxide synthase (eNOS), cyclooxygenases (COX)] by immunoblotting. Triiodothyronine (T3) caused concentration-dependent (3×10−6–3×10−5 M) relaxations in mesenteric (pEC50, 4.96±0.19) and femoral (pEC50, 4.57±0.35) arteries without endothelium. In femoral arteries of rats with diabetes, 5-methylamino-2-[[(2S,3R,5R,8S,9S)-3,5,9-trimethyl-2-(1-oxo-(1H-pyrrol-2- -yl)propan-2-yl)-1,7-dioxaspiro-(5,5)undecan-8-yl]methyl]benzooxazole-4-carboxylic acid (A23187, 3×10−7 to 10−6 M) caused partly endothelium-dependent contractions. After chronic T3-treatment with (10 μg/kg/day; four weeks), the contractions to A23187 of preparations with and without endothelium were comparable, the thromboxane B2-release was reduced (by 38.1±9.2%). The pEC50 of 9, 11-dideoxy-11α, 9α-epoxymethanoprostaglandin F2α (U46619, TP-receptor agonist) was increased in T3-treated diabetic rats compared with controls (8.53±0.06 vs 7.94±0.09). The protein expression of eNOS increased (by 228%) but that of COX-1 decreased (by 35%) after chronic T3 treatment. In human umbilical vein endothelial cells incubated for one week with T3 (10−10–10−7 M) in the presence but not in the absence of interleukin-1β (1 ng/ml), the expression of eNOS was increased compared to control. In conclusion, thyroid hormone acutely relaxes mesenteric and femoral vascular smooth muscle, but given chronically reduces the release of endothelium-derived vasoconstrictor prostanoids while enhancing the responsiveness of TP receptors of vascular smooth muscle.
Persistent Identifierhttp://hdl.handle.net/10722/209799
ISSN
2015 Impact Factor: 2.73
2015 SCImago Journal Rankings: 1.115

 

DC FieldValueLanguage
dc.contributor.authorCai, Y-
dc.contributor.authorManio, MM-
dc.contributor.authorLeung, GPH-
dc.contributor.authorXu, A-
dc.contributor.authorTang, EHC-
dc.contributor.authorVanhoutte, PMGR-
dc.date.accessioned2015-05-18T03:24:35Z-
dc.date.available2015-05-18T03:24:35Z-
dc.date.issued2015-
dc.identifier.citationEuropean Journal of Pharmacology, 2015, v. 747, p. 18-28-
dc.identifier.issn0014-2999-
dc.identifier.urihttp://hdl.handle.net/10722/209799-
dc.description.abstractHypothyroidism impairs endothelium-dependent dilatations, while hyperthyroidism augments the production of endothelial nitric oxide. Thus, experiments were designed to determine if thyroid hormone causes endothelium-dependent responses, or alleviates diabetic endothelial dysfunction. Isometric tension was measured in rings with or without endothelium of arteries from normal and diabetic Sprague-Dawley rats. Release of 6-keto prostaglandin F1α and thromboxane B2 were measured by enzyme linked immunosorbent assay and protein levels [endothelial nitric oxide synthase (eNOS), cyclooxygenases (COX)] by immunoblotting. Triiodothyronine (T3) caused concentration-dependent (3×10−6–3×10−5 M) relaxations in mesenteric (pEC50, 4.96±0.19) and femoral (pEC50, 4.57±0.35) arteries without endothelium. In femoral arteries of rats with diabetes, 5-methylamino-2-[[(2S,3R,5R,8S,9S)-3,5,9-trimethyl-2-(1-oxo-(1H-pyrrol-2- -yl)propan-2-yl)-1,7-dioxaspiro-(5,5)undecan-8-yl]methyl]benzooxazole-4-carboxylic acid (A23187, 3×10−7 to 10−6 M) caused partly endothelium-dependent contractions. After chronic T3-treatment with (10 μg/kg/day; four weeks), the contractions to A23187 of preparations with and without endothelium were comparable, the thromboxane B2-release was reduced (by 38.1±9.2%). The pEC50 of 9, 11-dideoxy-11α, 9α-epoxymethanoprostaglandin F2α (U46619, TP-receptor agonist) was increased in T3-treated diabetic rats compared with controls (8.53±0.06 vs 7.94±0.09). The protein expression of eNOS increased (by 228%) but that of COX-1 decreased (by 35%) after chronic T3 treatment. In human umbilical vein endothelial cells incubated for one week with T3 (10−10–10−7 M) in the presence but not in the absence of interleukin-1β (1 ng/ml), the expression of eNOS was increased compared to control. In conclusion, thyroid hormone acutely relaxes mesenteric and femoral vascular smooth muscle, but given chronically reduces the release of endothelium-derived vasoconstrictor prostanoids while enhancing the responsiveness of TP receptors of vascular smooth muscle.-
dc.languageeng-
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/ejphar-
dc.relation.ispartofEuropean Journal of Pharmacology-
dc.rightsNOTICE: this is the author’s version of a work that was accepted for publication in European Journal of Pharmacology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in European Journal of Pharmacology, 2015, v. 747, p. 18-28 DOI: 10.1016/j.ejphar.2014.11.036-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleThyroid hormone affects both endothelial and vascular smooth muscle cells in rat arteries-
dc.typeArticle-
dc.identifier.emailLeung, GPH: gphleung@hkucc.hku.hk-
dc.identifier.emailXu, A: amxu@hkucc.hku.hk-
dc.identifier.emailTang, EHC: evatang1@hku.hk-
dc.identifier.emailVanhoutte, PMGR: vanhoutt@hku.hk-
dc.identifier.authorityLeung, GPH=rp00234-
dc.identifier.authorityXu, A=rp00485-
dc.identifier.authorityTang, EHC=rp01382-
dc.identifier.authorityVanhoutte, PMGR=rp00238-
dc.description.naturepostprint-
dc.identifier.doi10.1016/j.ejphar.2014.11.036-
dc.identifier.hkuros243117-
dc.identifier.volume747-
dc.identifier.spage18-
dc.identifier.epage28-
dc.publisher.placeNetherlands-

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