Chronic propranolol administration impairs glucagon release during insulin-induced hypoglycemia in normal man.
Failure of a plasma glucagon rise in response to insulin-induced hypoglycemia was demonstrated in normal subjects taking therapeutic doses of the nonselective beta-adrenergic blocker, propranolol, for 7 days before testing. This is the first study to examine glucose homeostasis in normal subjects exposed to chronic propranolol therapy and helps to explain the development of spontaneous hypoglycemia in patients, either diabetic or nondiabetic, during beta-adrenergic receptor blockade. Previous studies of the acute parenteral effects of propranolol administration failed to show any significant effect on glucagon secretory dynamics in response to insulin-induced hypoglycemia. In the present study, however, chronic oral administration of propranolol resulted in severe impairment of the expected glucagon rise in response to hypoglycemia and was associated with severe hypoglycemia in one normal subject.
D000328:Adult; D005934:Glucagon / Q000097:blood*; D013006:Growth Hormone / Q000097:blood; D006801:Humans; D007003:Hypoglycemia / Q000097:blood / Q000139:chemically induced*; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D011433:Propranolol / Q000008:administration & dosage / Q000009:adverse effects*; D013997:Time Factors
D007328:Insulin; D013006:Growth Hormone; D005934:Glucagon; D011433:Propranolol