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1 Department of Pharmacology, Michigan State University, East Lansing, Michigan
The purpose of the present study was to determine the effect of triiodothyronine (T3) pretreatment on amine-induced rat cardiac phosphorylase activation and to determine whether the thyroid-amine interaction could be explained on the basis of blockade of amine uptake. Pretreatment of rats with T3 (500 mg/kg daily for 3 days) resulted in an increase in cardiac phosphorylase a. In addition, the animals showed a marked enhancement of the effect of norepinephrine, isoproterenol or tyramine infusion on cardiac phosphorylase a. The administration of cocaine to T3-pretreated animals resulted in a further enhancement of the norepinephrine effect but not of the isoproterenol effect. Pretreatment of animals with reserpine did not affect control enzyme levels or the response to norepinephrine in control animals but did decrease phosphorylase a in T3-pretreated animals to control levels. Animals pretreated with reserpine and T3 exhibited a marked sensitivity to norepinephrine. All increases in phosphorylase a caused by drug treatments could be blocked or decreased by propranolol. The propranolol blockade was unaffected by atropine. It is concluded that T3 pretreatment potentiates the effect of norepinephrine, isoproterenol and tyramine on phosphorylase a. T3 potentiation is not the result of blockade of amine uptake.
Submitted on November 27, 1967