Changes in cardiac glycogen synthase and phosphorylase activities following stimulation of beta-adrenergic receptors in rats.

Following a subcutaneous injection of isoprenaline into rats (5 mg X kg-1 b.w.) the cardiac glycogen stores were depleted by about 90% in less than 15 min. Complete restoration of myocardial glycogen was slow (more than 7-8 hours) despite an elevated glycogen synthase activity. A cardioselective beta-adrenergic receptor blockade (using atenolol) resulted in a complete restoration of glycogen stores in 30 min. The results indicate that the potential of myocardial tissue for glycogenogenesis is great but this capability is obscured by continuous glycogenolysis induced by a long-term activation of phosphorylase. The relative importance of beta-receptor stimulation and actual glycogen level in the control of cardiac synthase is discussed.