Open AccessThyroid hormone stimulates NO production via activation of the PI3K/Akt pathway in vascular myocytes
Author(s) -
Maria Alícia Carrillo-Sepúlveda,
Graziela Scalianti Ceravolo,
Z. B. Fortes,
Maria Helena Catelli de Carvalho,
Rita C. Tostes,
Francisco Rafael Martins Laurindo,
R. Clinton Webb,
Maria Luiza Morais BarretoChaves
Publication year - 2009
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvp304
Subject(s) - vascular smooth muscle , protein kinase b , pi3k/akt/mtor pathway , endocrinology , medicine , phosphorylation , nitric oxide synthase , biology , blot , phenylephrine , signal transduction , nitric oxide , chemistry , microbiology and biotechnology , biochemistry , gene , blood pressure , smooth muscle
Thyroid hormone (TH) rapidly relaxes vascular smooth muscle cells (VSMCs). However, the mechanisms involved in this effect remain unclear. We hypothesize that TH-induced rapid vascular relaxation is mediated by VSMC-derived nitric oxide (NO) production and is associated with the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signalling pathway.
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