Successive epinephrine infusions were used as a partial model to examine hormonal and metabolic responses to repeated stress stimuli. As both the endogenous opiates and epinephrine are released in response to stress, we have also studied interactions between epinephrine and B-endorphin. Epinephrine (0.1 μg/kg · min) was infused for 60 min, followed by a 60-min recovery, a second 60 min of epinephrine, and a 60-min recovery, in nine normal, conscious dogs. In a similar study, B-endorphin (0.06 μg/kg · min) was given 30 min before epinephrine, then continuously infused throughout the study (N = 4 dogs). When epinephrine was infused, levels rose to 600–800 pg/ml. The changes in glucagon, B-endorphin, FFA, and hepatic glucose production were similar during both epinephrine infusions, but there was a diminished insulin response, a greater decrease in glucose metabolic clearance, and a greater increase in plasma glucose with the second epinephrine infusion. When B-endorphin was given, plasma levels increased to 5.3 ng/ml. Compared with the infusion of epinephrine alone, there was a much greater rise in plasma glucose due to greater suppression of glucose metabolic clearance. With the second epinephrine infusion, however, the changes in glucose concentration were not substantially different from those seen during the second infusion of epinephrine alone, as both hepatic glucose production and glucose metabolic clearance were suppressed. B-endorphin diminished the insulin and glucagon responses during the first epinephrine infusion and abolished them during the second, but did not alter the FFA, ACTH, or cortisol responses to epinephrine.

Thus, (1) successive epinephrine infusions appear to desensitize the B-cells, resulting in a greater hypergly-cemic response due to exaggerated suppression of MCR, and (2) B-endorphin (0.06 jig/kg min) attenuated epinephrine's effects on the pancreatic A- and B-cells, and enhanced epinephrine's hyperglycemic effects by potentiating its inhibitory effect on MCR and modulating its stimulatory effects on the liver, through direct and/or indirect mechanisms.

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