Role of the renin-angiotensin system in cardiac hypertrophy induced in rats by hyperthyroidism

Hiroyuki Kobori, Atsuhiro Ichihara, Hiromichi Suzuki, Tsuneo Takenaka, Yutaka Miyashita, Matsuhiko Hayashi, Takao Saruta

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This study was conducted to examine whether the renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy without involving the sympathetic nervous system. Sprague-Dawley rats were divided into control-innervated, control-denervated, hyperthyroid-innervated, and hyper thyroid-denervated groups using intra-peritoneal injections of thyroxine and 6-hydroxydopamine. After 8 wk, the heart-to-body weight ratio increased in hyperthyroid groups (63%), and this increase was only partially inhibited by sympathetic denervation. Radioimmunoassays and reverse transcription- polymerase chain reaction revealed increased cardiac levels of renin (33%) and angiotensin II (53%) and enhanced cardiac expression of renin mRNA (225%) in the hyperthyroid groups. These increases were unaffected by sympathetic denervation or 24-h bilateral nephrectomy. In addition, losartan and nicardipine decreased systolic blood pressure to the same extent, but only losartan caused regression of thyroxine-induced cardiac hypertrophy. These results suggest that thyroid hormone activates the cardiac renin-angiotensin system without involving the sympathetic nervous system or the circulating renin-angiotensin system; the activated renin-angiotensin system contributes to cardiac hypertrophy in hyperthyroidism.

Original languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number2 42-2
Publication statusPublished - 1997


  • Angiotensin II type 1 receptor antagonist
  • Chemical sympathectomy
  • Polymerase chain reaction
  • Tissue renin

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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