To determine the possible role of adrenergic mechanisms in mediating the fall in serum potassium concentration after intravenous injection of insulin.

Research Design and Methods

Eighteen nondiabetic male volunteers, divided into three groups of six subjects, comprised the study. Hypoglycemia was induced by a bolus of short-acting insulin (0.15 U∕kg body wt). Six subjects were studied in control conditions, six during α-adrenergic blockade with phentolamine, and six during β-adrenergic blockade with propranolol.


In the control group, there was an immediate fall in serum potassium from 4.0 ± 0.1 to 3.6 ± 0.1 mM at baseline + 15 min. After the onset of acute hypoglycemia, potassium decreased further in the control group, reaching a lowest concentration of 3.3 ± 0.1 mM. In the propranolol group, the late decrease in potassium was inhibited, and there were no further changes in serum potassium. During α-blockade, there was an exaggerated fall to 2.6 ± 0.1 mM at 30 min after the onset of hypoglycemia.


The later fall in serum potassium, which occurs after the onset of hypoglycemia, is probably mediated by stimulation of β-adrenoreceptors, whereas coincidental stimulation of α-adrenoreceptors opposes this fall in potassium and may prevent the development of severe hypokalemia in response to acute hypoglycemia.

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