Thyroid hormone regulation of cardiac glycogen metabolism

Abstract

The administration of thyroxin to rats (500 [mu]g daily for 2-3 weeks, 500 [mu]g daily for 1 week, or 50 [mu]g daily for 2 weeks) or triiodothyronine (100 [mu]g daily for 3-5 days) increased cardiac phosphorylase a levels. Total cardiac phosphorylase activity was unchanged. Pretreatment with reserpine prevented and the [beta]-adrenergic blocking agents reduced this thyroxin-induced increase in phosphorylase a. Thyroxin or triiodothyronine treatment potentiated the response of cardiac phosphorylase to exogeneously administered catecholamines. This enhancement of the catecholamine-induced increase in phosphorylase a could be clearly demonstrated after the animals were pretreated with reserpine. Dose-response relationships for these agents are illustrated. Glycogen analyses on the same hearts indicated a parallelism between the increase in phosphorylase a and the reduction in glycogen content. While hearts of thyroidectomized animals showed a decrease in phosphorylase a levels and an increase in glycogen relative to controls, the response after catecholamines was unchanged. These data suggest that thyroxin may enhance these catecholamine responses by modulation of the myocardial metabolic adrenergic receptor.