Catecholamine stimulation of hepatic glycogenolysis during anoxia in the turtle Chrysemys picta.

Abstract

The remarkable tolerance of some species of turtles to anoxia is well documented. The role that hormones play in this anoxia tolerance, however, is poorly understood. This study examined the role of catecholamines in the mobilization of liver glycogen during anoxic submergence in painted turtles (Chrysemys picta). Turtles were subjected to 4 h of submergence anoxia or air (normoxic controls) and received injections of propranolol, a beta-adrenergic receptor antagonist, or saline. The results indicated that the catecholamines function during anoxia to increase blood glucose levels by stimulating hepatic glycogenolysis through an increase in both the total activity of glycogen phosphorylase and the percent a form. Anoxic turtles given propranolol showed a decrease in the percent a form of glycogen phosphorylase compared with control turtles given propranolol, indicating that anoxia per se or a correlate of anoxia may depress hepatic glycogenolysis. Catecholamines may counteract this depressant effect. Hepatic glycogen mobilization during anoxia appeared to be stimulated via beta-adrenergic receptors, as propranolol was effective in blocking the stimulation, whereas phentolamine, an alpha-receptor antagonist, was not.