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1 Department of Pharmacology, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
In rats, the administration of thyroxine or triiodothyronine caused an increase in cardiac phosphorylase a activity which was concomitant with an elevation in mean arterial blood pressure and an increase in heart rate. The cardiovascular stimulation and increase in phosphorylase activity observed after intravenous injection of epinephrine were not potentiated by prior intramuscular administration of thyroxine. Acetylcholine or pronethalol reversed the thyroxine-induced elevation of heart phosphorylase a activity and heart rate; reserpine inhibited the increase in cardiac phosphorylase a activity and the cardiovascular stimulation seen with thyroxine administration.
Accepted on January 26, 1965