Abstract
In a frequently cited paper Sokal , Sarcione and Henderson (1964) doubted the physiological glycogenolytic role of adrenaline (A). By using isolated perfused rat livers, they found adrenaline to be effective at doses higher than 140 ng/ml while a mere tenfold increase in glucagon leads to expressed glycogenolysis. Our in vivo experiments carried out with controlled release systems for adrenaline show that marked glycogenolysis takes place at an adrenaline serum level of not more than 20 ng/ml while endogenous glucagon levels do not differ from controls. We think, that the reason for those controversial results lies in the fact that Sokal , Sarcione and Henderson (1964) diminished the glycogenolytic action of adrenaline by blocking its alpha-component for the reason of an easier perfusion, and they further diminished its glycogenolytic action by omitting corticosterone, which is well known for its permissive role in adrenaline induced glycogenolysis in vivo.
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