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Diabetes Care, Vol 14, Issue 7 548-552, Copyright © 1991 by American Diabetes Association

ARTICLES

Effects of adrenergic blockade on serum potassium changes in response to acute insulin-induced hypoglycemia in nondiabetic humans

BM Fisher, I Thomson, DA Hepburn and BM Frier
Diabetic Department, Western Infirmary/Gartnavel General Hospital, Glasgow, Scotland, UK.

OBJECTIVE: 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 alpha-adrenergic blockade with phentolamine, and six during beta-adrenergic blockade with propranolol. RESULTS: 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 alpha-blockade, there was an exaggerated fall to 2.6 +/- 0.1 mM at 30 min after the onset of hypoglycemia. CONCLUSIONS: The later fall in serum potassium, which occurs after the onset of hypoglycemia, is probably mediated by stimulation of beta-adrenoreceptors, whereas coincidental stimulation of alpha-adrenoreceptors opposes this fall in potassium and may prevent the development of severe hypokalemia in response to acute hypoglycemia.
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I. Bin-Jaliah, P. D. Maskell, and P. Kumar
Indirect sensing of insulin-induced hypoglycaemia by the carotid body in the rat
J. Physiol., April 1, 2004; 556(1): 255 - 266.
[Abstract] [Full Text] [PDF]


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Copyright © 1991 by the American Diabetes Association.