Hormonal control of glycogenolysis and the mechanism of action of adrenaline in amphibian liver in vitro.

In in vitro cultures of liver from Ambystoma mexicanum glycogenolysis was stimulated by adrenaline, glucagon, and vasopressin in a dose-dependent manner. Maximum activity was seen at 10(-6) M hormone while 10(-9) M was without effect. Dibutyryl cyclic AMP (10(-3) M) stimulated glycogenolysis maximally although 10(-5) M had no effect. The glucose release brought about by adrenaline was blocked by the beta-adrenergic antagonist propranolol but not by prazosin or yohimbine which are alpha 1- and alpha 2-adrenergic antagonists. Cyclic AMP concentrations in liver were elevated within 1 min of administration of adrenaline and remained elevated for at least 60 min. Phosphorylase a activity was elevated 10 min after addition of adrenaline and remained elevated for at least 6 hr. The rise in hepatic cyclic AMP concentration and phosphorylase a activity was largely blocked by propranolol. These findings are consistent with adrenaline acting via a beta-adrenergic receptor in A. mexicanum. Glycogenolysis in A. mexicanum liver was stimulated by isoprenaline and phenylephrine and in each case the stimulation was reduced in the presence of propranolol but unaffected by phentolamine. High concentrations of methoxamine, a specific alpha 1-agonist, had no effect upon glycogenolysis. These findings suggest that alpha-adrenergic receptors play no role in regulation of glycogenolysis in A. mexicanum.