Effects of Adrenal Cortical Hormones and Thyroxine on Phosphorylase Activity in Muscle

The open-chest rat preparation was used to investigate the interaction between corticosterone and thyroxine in regulating myo-cardial phosphorylase activity; measurements were also made of heart rate and mean arterial blood pressure. Corticosterone, but not thyroxine, caused an increase in total heart phos-phorylase which was due to a specific increase in the enzyme rather than a general increase in cellular protein. Both corticosterone and thyroxine increased cardiac phosphorylase a activity n i normal rats. The enzymatic and positive chronotropic effects of thyroxine were markedly diminished in adrenalectomized rats; simultaneous administration of corticosterone with thyroxine restored the responses to normal. In thy-roidectomized animals, corticosterone produced less stimulation of heart phosphorylase a than in control rats. When both thyroxine and corti-costerone were given to thyroidectomized animals, the level of phosphorylase a approximated that seen when these hormones were injected into normal rats. Pretreatment of rats with cortisol or corticosterone did not increase phosphorylase a activity in isolated skeletal muscle (rat diaphragm). Unlike heart muscle, prior treatment with glucocorticoids did not potentiate an epinephrine-induced rise of phosphorylase a activity in rat diaphragm. It is concluded that, in order for thyroxine to exert its optimal stimulatory effect on cardiac phosphorylase a activity and heart rate in rats, the presence of corticosterone is necessary. Similarly, the increase in phos-phorylase a activity in the heart produced by corticosterone is best demonstrated in the presence of thyroxine. Skeletal muscle responds to glucocorticoids differently from cardiac muscle i n that, in the former, administration of corti-costerone does not increase phosphorylase a activity or potentiate the epinephrine-induced rise in this enzyme. (Endocrinology84: 1107, 1969)