THE EFFECT OF CATECHOLAMINES ON MUSCLE GLYCOGEN AND PHOSPHORYLASE ACTIVITY

¹ The University of Michigan Medical School, Ann Arbor, Michigan

Epinephrine (500 µg/kg, s.c.) caused an increase in skeletal muscle phosphorylase a and a decrease in glycogen content in the rat. The phosphorylase response was maximal 5 minutes after injection and was sustained throughout the 1-hour sampling period. There was no effect on either cardiac phosphorylase a or glycogen levels. After phenoxybenzamine pretreatment, subcutaneous epinephrine caused an increase in e ardiac phosphorylase a levels and a decrease in cardiac glycogen content. Although skeletal muscle and cardiac phosphorylase were activated to a similar degree, the rate and magnitude of the glycogen loss were greater in the heart than those observed in skeletal muscle. The epinephrine response after phenoxybenzamine pretreatment could be correlated with increased plasma epinephrine levels.

Norepinephrine (500 µg/kg, s.c.) was without effect on either cardiac or skeletal muscle phosphorylase or glycogen at all times up to 1 hour after injection. After phenoxybenzamine pretreatment, norepinephrine produced a cardiac response similar to that of epinephrine, while only a moderate response was observed in skeletal muscle.

Isoproterenol (50 µg/kg, s. c.) gave responses in cardiac and skeletal muscle which were similar to those observed after epinephrine in phenoxybenzamine-treated animals for both phosphorylase activation and glycogen loss. Isoproterenol was the most potent catecholamine for both cardiac phosphorylase activation and glycogen loss.

An increase in phosphorylase a levels preceded the tissue glycogen loss in both heart and skeletal muscle after catecholamine administration. While there was an inverse correlation between phosphorylase activation and glycogen levels in heart and skeletal muscle at certain times after catecholamine administration, the data also indicated that factors other than the tissue phosphorylase a level may determine the rate and magnitude of the glycogen loss.

Dichloroisoproterenol blocked both the cardiac phosphorylase activation and glycogen loss after subcutaneous or intravenous administration of catecholamines.

Increased or decreased tissue catecholamine levels were without effect on cardiac phosphorylase a values. Reserpine increased the cardiac glycogen content.

Chronic thyroxin treatment increased cardiac phosphorylase a levels and decreased the cardiac glycogen content. Skeletal muscle phosphorylase and glycogen were not affected by thyroxin treatment.