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This Article Full Text Full Text (PDF) All Versions of this Article: 285/6/R1473    most recent 00269.2003v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (15) Citing Articles via Google Scholar Google Scholar Articles by Hu, L. W. Articles by Barreto-Chaves, M. L. M. Search for Related Content PubMed PubMed Citation Articles by Hu, L. W. Articles by Barreto-Chaves, M. L. M.

NEUROHUMORAL CONTROL OF CIRCULATION AND HYPERTENSION

Thyroxine-induced cardiac hypertrophy: influence of adrenergic nervous system versus renin-angiotensin system on myocyte remodeling

¹Department of Anatomy and ²Department of Histology and Embryology, Institute of Biomedical Sciences, Universidade de São Paulo, São Paulo 05508-900; and ³Heart Institute (InCor) University of São Paulo Medical School, São Paulo 05403-000, Brazil

Submitted 14 May 2003 ; accepted in final form 18 August 2003

The present study assessed the possible involvement of the renin-angiotensin system (RAS) and the sympathetic nervous system (SNS) in thyroxine (T₄)-induced cardiac hypertrophy. Hemodynamic parameters, heart weight (HW), ratio of HW to body weight (HW/BW), and myocyte width were evaluated in absence of thyroid hormone (hypothyroidism) and after T₄ administration. Male Wistar rats were used. Some were subjected to thyroidectomies, whereas hyperthyroidism was induced in others via daily intraperitoneal injection of T₄ (25 or 100 µg · 100 g BW^-1 · day^-1) for 7 days. In some cases, T₄ administration was combined with the angiotensin I-converting enzyme inhibitor enalapril (Ena), with the angiotensin type 1 (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 by administration of either T₄ alone or T₄ in combination with the specific inhibitors. However, SBP decreased significantly in hypothyroid rats. An increased heart rate was seen after administration of either T₄ alone or T₄ in combination with either Los or Ena. Although the higher dose of T₄ significantly increased HW, HW/BW 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 T₄-induced cardiac hypertrophy is associated with both the SNS and the RAS.

cardiac myocytes; thyroid hormone; angiotensin-converting enzyme; angiotensin II receptors

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