Specific beta-adrenergic mechanisms in the hypoglycaemic activation of gastrin and gastric acid secretion.
To study whether specific beta-adrenergic mechanisms contribute to the hypoglycaemic activation of gastrin and gastric acid secretion, the effects of racemic and dextroisomer propranolol (0.1 mg/kg, intravenously) were studied during insulin tests (0.2 IU/kg) in 13 persons. dl-Propranolol inhibited the gastrin response to hypoglycaemia markedly and more than the insignificant alteration observed after d-propranolol. Gastric acid response to hypoglycaemia was significantly reduced by dl-propranolol and not by d-propranolol. The findings demonstrate that non-beta-adrenergic effects of propranolol on the stomach are minor and that specific beta-adrenergic mechanisms are directly or indirectly involved in the hypoglycaemic stimulation of the stomach.
D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005755:Gastrins / Q000097:blood*; D006801:Humans; D007003:Hypoglycemia / Q000097:blood*; D007328:Insulin; D008297:Male; D008875:Middle Aged; D011433:Propranolol / Q000494:pharmacology*; D013237:Stereoisomerism
D001786:Blood Glucose; D005755:Gastrins; D007328:Insulin; D011433:Propranolol