Adrenergic mechanisms in recovery from hypoglycemia in man: adrenergic blockade.

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Abstract
Simultaneous glucose and alanine turnover rates, along with static measurements of counterregulatory hormones and selected metabolic intermediates, were determined during insulin-induced hypoglycemia in normal subjects infused with saline, phentolamine (an .alpha.-adrenergic blocking agent), and propranolol (a .beta.-adrenergic blocking agent) in separate experiments. In the control studies plasma glucose fell from 87 .+-. 4 to 35 .+-. 4 mg/dl 30 min after i.v. crystalline insulin (0.05 u[units]/kg). Glucose utilization doubled and then returned to baseline by 40 min, whereas glucose production fell initially, began to rise by 30 min, and reached maximal rates twice baseline by 40 min after insulin. Hypoglycemia was associated with increments in plasma epinephrine, norepinephrine, glucagon, growth hormone and cortisol; blood lactate rose transiently after insulin injection, whereas blood .beta.-hydroxybutyrate was suppressed initially but rose during glucose recovery. Despite hemodynamic and metabolic evidence of .alpha.- and .beta.-adrenergic blockade during the infusion of phentolamine and of propranolol, respectively, base-line and postinsulin plasma glucose concentrations, glucose utilization and production rates, and rates of glucose formation from alanine did not differ from those of the control study. Adrenergic mechanisms do not appear to play a primary role in recovery from insulin-induced hypoglycemia in man, but they do appear to play a secondary role since they become critical to recovery from hypoglycemia only in the absence of other counterregulatory mechanisms.