On the beta-adrenergic contribution to the gastric acid and gastrin responses to hypoglycaemia in man.
To study the beta-adrenergic contribution to the hypoglycaemic stimulation of gastric acid and gastrin release the effect of an equal and extensive beta-adrenergic blockade with three drugs was studied. Propranolol was investigated in 12, pindolol in 22, and practolol in 11 patients. Fasting concentration of gastrin serum and spontaneous acid secretion were not reduced by the drugs. Propranolol eliminated the gastrin response to hypoglycaemia, pindolol reduced it, and practolol caused no alteration. The hypoglycaemic acid response was reduced by all three drugs, propranolol reduced the response to one-half and was the strongest inhibitor, practolol the weakest. It is concluded that beta-adrenergic receptors may be of major importance for the hypoglycaemic stimulation of the stomach, but the receptors respond differently from the receptors in the heart.
D000328:Adult; D000368:Aged; D001786:Blood Glucose / Q000032:analysis; D004381:Duodenal Ulcer / Q000097:blood / Q000503:physiopathology; D005260:Female; D005750:Gastric Juice / Q000378:metabolism*; D005755:Gastrins / Q000097:blood / Q000378:metabolism*; D006801:Humans; D007003:Hypoglycemia / Q000503:physiopathology*; D007328:Insulin / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D010869:Pindolol / Q000494:pharmacology; D011217:Practolol / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011941:Receptors, Adrenergic
D001786:Blood Glucose; D005755:Gastrins; D007328:Insulin; D011941:Receptors, Adrenergic; D011433:Propranolol; D010869:Pindolol; D011217:Practolol