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

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          Abstract

          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 hyperthyroid-denervated groups using intraperitoneal 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.

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          Author and article information

          Journal
          Am. J. Physiol.
          The American journal of physiology
          American Physiological Society
          0002-9513
          0002-9513
          Aug 1997
          : 273
          : 2 Pt 2
          Affiliations
          [1 ] Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
          Article
          NIHMS73974
          10.1152/ajpheart.1997.273.2.H593
          2574495
          9277473
          4bc81775-17fa-4d24-ad32-acffbfec1300
          History

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