Effect of thyroidectomy on rat T-kininogen.
The thyroid state affects the inflammatory reaction; in general, thyroid hormones increase and hypothyroidism decreases the inflammatory response. T-kininogen is an acute phase protein that inhibits cysteine proteases. The influence of thyroidectomy and 3,5,3'-triiodothyronine (T3)-treatment of thyroidectomized animals was examined on rat plasma T-kininogen concentration. Thyroidectomy increased the T-kininogen level three- to fourfold. A single administration of 10 micrograms T3/100 g body wt in 7-wk postthyroidectomy rats decreased it by approximately 50%. Daily treatment with 0.5 micrograms T3/100 g body wt prevented the increases in T-kininogen. The modifications in plasma T-kininogen concentration were confirmed by high-performance liquid chromatography analysis of the plasma kinins released by trypsin. They demonstrated that T-kinin was greatly and bradykinin slightly increased after thyroidectomy and that T-kinin concentration in T3-treated thyroidectomized animals was almost restored to the control level. The ability of thyroidectomized animals to produce a higher plasma T-kininogen compared with euthyroid animals was further documented when T-kininogen production was stimulated by laparotomy. This procedure resulted in a fourfold increase in T-kininogen in thyroidectomized animals compared with controls. The increase of plasma T-kininogen level after thyroidectomy results from a more active synthesis of the protein, since liver slices from thyroidectomized rats synthesized T-kininogen at a rate about two times higher than normal rats. These data may account at least in part for the diminution of the inflammatory response observed after thyroidectomy.