[Regulation of RNA synthesis in the rat heart in L-thyroxine toxicosis and hypothyroidism; the role of RNA-polymerases and the template activity of chromatin]. / Reguliatsiia sinteza RNK v serdtse krysy pri L-tiroksinovom toksikoze i gipotireoze; rol' RNK-polimeraz i matrichnoi aktivnosti khromatina.

It is shown that L-thyroxin applied to rats has induced in them development of pronounced cardiac hypertrophy accompanied by an increase in the total amount of nucleic acids in the myocardium (per organ) and enhancement of the RNA synthesis rate. It is confirmed by a considerable rise of the intensity of the labelled uridine incorporation into RNA without alteration of the specific radioactivity in a pool of free nucleotides and by the growth of the RNA-polymerase I activity. When L-thyroxin toxicosis lasts for four weeks and heart weight has not already increased the content of nucleic acids remains high, the rate of the label incorporation into RNA lowering down to the normal level. The activity of RNA-polymerase I is almost twice as low as that under thyrotoxicosis lasting for a week. In this case the matrix activity of chromatin tested by exogenous RNA-polymerase III of the rat gets lower. Under mercasolyl-induced hypothyrosis the heart weight decreases as well as the amount of nucleic acids, RNA synthesis intensity (by 40%) and RNA-polymerase I activity in it. The data obtained testify to the versatile effect of the thyroid hormones on RNA biosynthesis in the cardiac muscle and on the activity of both the RNA-polymerases and chromatin matrix.