Inhibition of sulphonylurea-stimulated insulin secretion by beta adrenergic blockage.
Normal dogs were injected i.v. with a single dose of 0.25 mg/kg sodium salt of HB 419 (Glibenclamide). Plasma insulin and glucose concentrations were measured at stated intervals over a period of two hours. The rise in insulin, but not the hypoglycemic response was abolished in peripheral blood when the animals were pretreated with a single i.v. injection of either 0.1 mg/kg or 0.3 mg/kg dl-propranolol, 30 min prior to the administration of HB 419. The d-isomer of propranolol was ineffective in this respect. These results indicate that a) the mechanism by which propranolol inhibits sulphonylurea-stimulated insulin secretion involves beta adrenergic receptors; and b) the hypoglycemia produced by HB 419 in the presence of propranolol could be the result of extrapancreatic effects. Since the possibility of an early rise in the insulin concentration of portal blood was not excluded in our present series of experiments, final proof will have to be provided by studies in totally pancreatectomized dogs.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D004285:Dogs; D005260:Female; D005905:Glyburide / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D007328:Insulin / Q000097:blood / Q000378:metabolism*; D000078790:Insulin Secretion; D008297:Male; D011433:Propranolol / Q000494:pharmacology*; D013237:Stereoisomerism
D001786:Blood Glucose; D007328:Insulin; D011433:Propranolol; D005905:Glyburide