Key result
Treatment with 3,3′,5-triiodo-L-thyronine (T3) in rats increased liver angiotensinogen mRNA by 2 to 3 times at 8 to 12 hours, followed by an elevation in plasma angiotensinogen concentration.
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Hypothesis-generating in rats; leaves open T3-angiotensinogen effects in human cardiovascular disease.
We studied the expression of angiotensinogen and renin genes in rats treated with 3,3′,5-triiodo-L-thyronine (T3) at doses of 0.1 and 1 mg/kg of body weight. Liver angiotensinogen mRNA increased by 2 to 3 times 8 to 12 hours after T3-treatment. This increase was dose-related. Plasma angiotensinogen concentration (PAC) increased 12 hours after T3-treatment. Brain and renal angiotensinogen mRNA levels and the renal renin mRNA level remained the same throughout the experimental periods. These results suggest that the thyroid hormone initially increases angiotensinogen mRNA and leads to an increase in the production of angiotensinogen in the liver followed by an elevation of PAC.
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Kimura et al. (1990) studied this question. 3,3′,5-triiodo-L-thyronine (T3) was evaluated on Liver angiotensinogen mRNA levels (2 to 3 times increase). Treatment with 3,3′,5-triiodo-L-thyronine (T3) in rats increased liver angiotensinogen mRNA by 2 to 3 times at 8 to 12 hours, followed by an elevation in plasma angiotensinogen concentration.
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