Potassium homeostasis during hyperinsulinemia: effect of insulin level, beta-blockade, and age

The euglycemic glucose clamp technique was used to evaluate the influence of level and duration of hyperinsulinemia, presence of beta-adrenergic blockade, and subject age on insulin-mediated changes in plasma potassium. In 16 young subjects, 2-h insulin infusions at 20 (n = 6), 80 (n = 13), and 200 (n = 8) mU.m-2.min-1 resulted in dose-dependent declines in plasma potassium (P less than 0.001 at all doses) during the 1st h. During the 2nd h plasma potassium declined during the 20 mU.m-2.m-1 infusions, was stable during the 80 mU.m-2.m-1 infusions, and rose slightly during the 200 mU.m-2.min-1 infusions. There was a significant reciprocal relationship between the changes in plasma potassium during the 1st and 2nd h of study (r = 0.99, P less than 0.01). During 4-h infusions (80 mU.m-2.min-1, n = 6) plasma potassium declined during the first 90 min (p less than 0.001) and rose thereafter until the end of the infusion (P less than 0.05). Studies with and without propranolol infusion at two insulin dose levels (20 and 80 mU.m-2.min-1) in six young subjects showed no effect of beta-blockade, and studies at three insulin dose levels [20 (n = 5), 80 (n = 6), and 200 (n = 6) mU.m-2.min-1 in 10 older males (63-77 yr] showed no effect of age on the changes in plasma potassium during hyperinsulinemia. These results suggest the presence of a regulatory mechanism influencing insulin-mediated alterations in plasma potassium. This mechanism appears uninfluenced by age or beta-adrenergic blockade.