EFFECT OF CATECHOLAMINES ON SMOOTH MUSCLE MOTILITY AND PHOSPHORYLASE ACTIVITY

Uterine motility and phosphorylase activity were measured simultaneously in isolated uterine segments after exposure to various catecholamines and adrenergic blocking agents. The isolated, estrogen-primed rat uterus was found to contain primarily beta inhibitory adrenergic receptors, but the presence of alpha excitatory receptors was also demonstrated. Epinephrine, norepinephrine and isoproterenol increased phosphoryhase a activity while depressing uterine motility. The catecholamine-induced uterine relaxation and phosphorylase activation were both prevented by pretreatment with beta adrenergic blocking agents, but neither response was affected by alpha receptor blocking agents. The smallest dose of epinephrine that inhibited uterine motility (6 x 10 -9 M) also significantly increased phosphorylase a activity. Therefore, the epinephrine-induced relaxation and phosphorylase activation appeared to be related, at least to the extent that they were both beta adrenergic effects. A nonspecific smooth muscle relaxant, nitroglycerin, had no effect on uterine phosphorylase activity, even though it completely inhibited uterine motility. This indicated that phosphorylase activation was not related to uterine relaxation per Se, but was a specific effect of the catechohamines. Whether the catecholamine-induced phosphorylase activation and uterine relaxation are causally related or independent phenomena cannot be decided from these experiments. Epinephrine was also found to depress spontaneous motility and to increase phosphorylase a activity in isolated guinea pig taenia coli. However, the phosphorylasc activation occurred after time relaxation, indicating that the enzyme activation is not a prerequisite for epinephrine-induced relaxation.