Effect of radio-thyroidectomy and thyroid hormone replacement therapy on cardiac protein kinase activity and ATP hydrolysis

The regulatory effect of thyroid hormone on cardiac protein kinase activity and ATP hydrolysis was studied in developing rats. Experimental hypothyroidism induced by a single intraperitoneal injection of 200 muCi of 131I led to a significant impairment of body and heart growth and elevated the activity of membrane-bound protein kinase (measured in the absence of cyclic AMP). However, a slight (11%) but statistically non-significant decrease was observed in soluble protein kinase activity in hearts of hypothyroid rats. Furthermore, thyroid deficiency produced in neonatal life significantly decreased (34%) the rate of cardiac ATP hydrolysis. Treatment of thyroidectomized animals with L-triiodothyronine initiated early in life produced a time-dependent increase in heart weight as well as the activity of soluble protein kinase and the rate of ATP hydrolysis in cardiac tissue. Maximal rise in these parameters was observed in hypothyroid rats receiving L-triiodothyronine treatment for 24 days beginning from 7 days after radioiodine injection. These animals also showed a marked cardiac hypertrophy. In contrast, replacement therapy with L-triiodothyronine produced a decrease in the activity of the membrane-bound protein kinase, which seemed to be inversely proportional to the duration of L-triiodothyronine treatment. Our data provide evidence suggesting that thyroid hormone plays an important role in controlling ATP turnover in hearts of developing rats.