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Mechanisms related to the thyroid hormone (TH)‐induced vasorelaxation: contribution of reactive oxygen species (ROS) and purinergic signaling
Author(s) -
Basso Cristina Ribas Fürstenau,
Barreto-Chaves Maria Luiza Morais
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1140.11
Subject(s) - nox4 , endocrinology , medicine , purinergic receptor , reactive oxygen species , nox1 , hormone , western blot , chemistry , in vivo , thyroid , nadph oxidase , biology , oxidative stress , receptor , biochemistry , microbiology and biotechnology , gene
This study aims to determine the contribution of ROS and purinergic signaling to the TH‐induced vasorelaxation. In vitro (T3 added to VSMC primary culture) and in vivo (experimental hyperthyroidism developed in rats) protocols were performed to evaluate Nox1 and 4, and P2Y1,2, and 6 expression by Western blot. Preliminary results show that T3 (10‐7 M for 24 hours) diminished both Nox1 and Nox4 expression in VSMC (n=3). The experimental hyperthyroidism was confirmed by classical cardiac hypertrophy induced by T3 treatment (7 ìg/100 g body weight/day, 14 days ) since the ratio body weight (g)/ tibia's length (mm) was significantly higher in hyperthyroid rats (33.17 ± 3.34, n=15 vs 27.49 ± 2.24, n=14 in control group, p<0.05). Besides, total T4 levels measured in blood serum were significantly diminished in hyperthyroid animals (4.88 ± 0.599 in control group vs non‐detectable levels in T3‐treated rats), confirming that the feedback loop in TH production and secretion was satisfactorily working. Analysis of protein expression showed a diminution in P2Y6 expression and a modulation in Nox4 expression in hyperthyroid rats. Although additional experiments need to be performed, the present data point out the participation of both systems (ROS production and purinergic signalling) in the TH‐induced vasorelaxation. Source of research support: FAPESP and CNPq.