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Role of the Angotensin II Type 2 Receptor in thyroid hormone‐induced cardiac hypertrophy in a model of Ischemia/Reperfusion
Author(s) -
SILVA IVSON BEZERRA,
SANTOS ROBSON SOUZA,
BARRETOCHAVES MARIA LUÍZA MORAIS
Publication year - 2013
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.27.1_supplement.682.11
Subject(s) - endocrinology , medicine , knockout mouse , chemistry , protein kinase b , saline , receptor , muscle hypertrophy , ischemia , blot , radioimmunoassay , phosphorylation , biochemistry , gene
We hypothesize that the cardioprotective effect of TH in ischemia/reperfusion (I/R) model may occur with the participation of AT2R. Mice were subdivided in four different groups: 1) Wild‐Type (treated with saline); 2) Hyperthyroid (treated with T3 0.7 μg/Kg BW/day, i.p., 14 days); 3) AT2R knockout (treated with saline) and 4) Knockout + T3 (treated with T3). Hearts were mounted on a Langendorff apparatus under a constant retrograde flow (2–2,5 ml/min) with oxygenated (95% O 2 , 5% CO 2 ) Krebs–Henseleit buffer, 37ºC. Cardiac hypertrophy was determined based on heart weight (mg)/tibia's length (mm) ratio. Total T4 levels were determined using a commercial radioimmunoassay kit and cardiac protein expression was analyzed by Western Blotting. Data (mean±SEM) were analyzed by Student's t test, considering p <0,05. T3 treatment was able to induced cardiac hypertrophy which was not changed by AT2R absence. Vasodilator effect of T3 treatment was observed in wild‐type mice while it was abolished in knockout mice. The p‐Akt (Thr 308) levels were significantly increased in T3 group compared to control group in wild‐type mice, but no difference was observed between knockout T3‐treated and AT2R knockout mice. These data point to a possible involvement of AT2R and Akt signaling pathway on cardioprotective effect induced by T3.