{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T05:57:15Z","timestamp":1790488635420,"version":"4.1.0"},"reference-count":44,"publisher":"The Endocrine Society","issue":"7","license":[{"start":{"date-parts":[[2021,5,17]],"date-time":"2021-05-17T00:00:00Z","timestamp":1621209600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["MO1018\/2-2"],"award-info":[{"award-number":["MO1018\/2-2"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100010068","name":"Faculty of Medicine, University of Duisburg-Essen","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100010068","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Context<\/jats:title>\n                  <jats:p>Hypothyroidism impairs cardiovascular health and contributes to endothelial dysfunction with reduced vasodilation. How 3,5,3\u2032-triiodothyronine (T3) and its receptors are involved in the regulation of vasomotion is not yet fully understood. In general, thyroid hormone receptors (TRs) either influence gene expression (canonical action) or rapidly activate intracellular signaling pathways (noncanonical action).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Objective<\/jats:title>\n                  <jats:p>Here we aimed to characterize the T3 action underlying the mechanism of arterial vasodilation and blood pressure (BP) regulation.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Mesenteric arteries were isolated from male rats, wild-type (WT) mice, TR\u03b1 knockout (TR\u03b1\u200a0) mice, and from knockin mice with a mutation in the DNA-binding domain (TR\u03b1\u200aGS). In this mutant, DNA binding and thus canonical action is abrogated while noncanonical signaling is preserved. In a wire myograph system, the isolated vessels were preconstricted with norepinephrine. The response to T3 was measured, and the resulting vasodilation (\u0394 force [mN]) was normalized to maximum contraction with norepinephrine and expressed as percentage vasodilation after maximal preconstriction with norepinephrine (%NE). Isolated vessels were treated with T3 (1\u2005\u00d7\u200510\u201315 to 1\u2005\u00d7\u200510\u20135 mol\/L) alone and in combination with the endothelial nitric oxide\u2013synthase (eNOS) inhibitor L-NG-nitroarginine methyl ester (L-NAME) or the phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin. The endothelium was removed to determine the contribution of T3 to endothelium-dependent vasodilation. The physiological relevance of T3-induced vasodilation was determined by in vivo arterial BP measurements in male and female mice.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>T3 treatment induced vasodilation of mesenteric arteries from WT mice within 2 minutes (by 21.5\u2005\u00b1\u20051.7%NE). This effect was absent in arteries from TR\u03b1\u200a0 mice (by 5.3\u2005\u00b1\u20050.6%NE, P\u2005&amp;lt;\u2005.001 vs WT) but preserved in TR\u03b1\u200aGS arteries (by 17.2\u2005\u00b1\u20051.1%NE, not significant vs WT). Inhibition of either eNOS or PI3K reduced T3-mediated vasodilation from 52.7\u2005\u00b1\u20054.5%NE to 28.5\u2005\u00b1\u20054.1%NE and 22.7\u2005\u00b1\u20052.9%NE, respectively. Removal of the endothelium abolished the T3-mediated vasodilation in rat mesenteric arteries (by 36.7\u2005\u00b1\u20055.4%NE vs 3.5\u2005\u00b1\u20056.2%NE). In vivo, T3 injection led to a rapid decrease of arterial BP in WT (by 13.9\u2005\u00b1\u20051.9 mm Hg) and TR\u03b1\u200aGS mice (by 12.4\u2005\u00b1\u20051.9 mm Hg), but not in TR\u03b1\u200a0 mice (by 4.1\u2005\u00b1\u20051.9 mm Hg).<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>These results demonstrate that T3 acting through noncanonical TR\u03b1 action affects cardiovascular physiology by inducing endothelium-dependent vasodilation within minutes via PI3K and eNOS activation.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1210\/endocr\/bqab099","type":"journal-article","created":{"date-parts":[[2021,5,17]],"date-time":"2021-05-17T13:54:19Z","timestamp":1621259659000},"source":"Crossref","is-referenced-by-count":17,"title":["Noncanonical Thyroid Hormone Receptor \u03b1 Action Mediates Arterial Vasodilation"],"prefix":"10.1210","volume":"162","author":[{"given":"Daniela","family":"Geist","sequence":"first","affiliation":[{"name":"Department of Endocrinology, Diabetes and Metabolism, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G Sebastian","family":"H\u00f6nes","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Diabetes and Metabolism, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janina","family":"Gassen","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Diabetes and Metabolism, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Helena","family":"Kerp","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Diabetes and Metabolism, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3576-3772","authenticated-orcid":false,"given":"Petra","family":"Kleinbongard","sequence":"additional","affiliation":[{"name":"Institute of Pathophysiology, West German Heart and Vascular Center, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7078-4160","authenticated-orcid":false,"given":"Gerd","family":"Heusch","sequence":"additional","affiliation":[{"name":"Institute of Pathophysiology, West German Heart and Vascular Center, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dagmar","family":"F\u00fchrer","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Diabetes and Metabolism, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9330-9036","authenticated-orcid":false,"given":"Lars C","family":"Moeller","sequence":"additional","affiliation":[{"name":"Department of Endocrinology, Diabetes and Metabolism, University Hospital Essen, University of Duisburg-Essen, 45147 Essen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"80","published-online":{"date-parts":[[2021,5,17]]},"reference":[{"issue":"21","key":"2021122820450114800_CIT0001","doi-asserted-by":"crossref","first-page":"21","DOI":"10.1186\/s12916-017-0777-9","article-title":"What is the association of hypothyroidism with risks of cardiovascular events and mortality? 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