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1 Department of Anatomy Biomedical Sciences Institute, University of Sao Paulo, Sao Paulo, SP, Brazil
2 Heart Institute (InCor), University of Sao Paulo Medical School, Sao Paulo, SP, Brazil
3 Department of Histology and Embryology, Universiy of Sao Paulo, Sao Paulo, SP, Brazil
* To whom correspondence should be addressed. E-mail: mchaves{at}usp.br.
The present study assesses the possible involvement of the renin-angiotensin system (RAS) and the sympathetic nervous system (SNS) in thyroxine-induced cardiac hypertrophy. Hemodynamic parameters, heart weight (HW), ratio of heart weight to body weight (HW/BW), and myocyte width were evaluated in absence of thyroid hormone (hypothyroidism) and after thyroxine (T4) administration. Male Wistar rats were used. Some were subjected to thyroidectomies, while hyperthyroidism was induced in others via daily intraperitoneal injection of L-thyroxine (25 or 100µg .100g-1 BW . day-1) for 7 days. In some cases, T4 administration was combined with the angiotensin I-converting enzyme inhibitor, enalapril (ENA), with the AT1 receptor blocker, losartan (LOS) or with the 
-adrenergic blocker, propanolol (PROP). Hemodynamics and morphology were then evaluated. Systolic blood pressure (SBP) was not altered either by administration of T4 alone or by T4 in combination with the specific inhibitors. However, SBP decreased significantly in hypothyroid rats. An increased heart rate was seen following administration of either T4 alone or T4 in combination with either LOS or ENA. Although the higher dose of T4 significantly increased HW, the HW/BW ratio increased in both T4-treated groups. ENA and PROP inhibited the increase in HW or HW/BW in hyperthyroid rats. Morphologically, both T4 dose levels significantly increased myocyte width, an occurrence prevented by RAS or SNS blockers. There was a good correlation between changes in HW/BW and myocyte width. These results indicate that thyroxine-induced cardiac hypertrophy is associated with both the SNS and the RAS.
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