Effect of a β₂-Sympathomimetic on Gastrin Release, Acid Secretion, and Blood Glucose During Basal Conditions and in Response to Insulin, 2-Deoxy-D-Glucose, and Feeding in the Dog

Abstract

The effect of a selective β₂-adrenoceptor agonist on basal volume and on insulin-, 2-deoxy-D-glucose (2-DG)-, and food-induced gastrin release was studied in conscious gastric fistula dogs. Acid output and blood glucose changes were also studied, except in the food experiments. Basal acid secretion and serum gastrin were unchanged after β₂-sympathetic infusion, whereas a slight increase in blood and glucose was found. The β₂-agonist almost prevented acid output and gastrin release after insulin hypoglycaemia. However, the hypoglycaemia was also inhibited. Gastric acid secretion stimulated by 2-DG was inhibited, as was probably the gastrin release. 2-DG increased the blood glucose level, and no significant differences were found after β₂ infusion. After feeding, gastrin release was initially decreased for one of five doses of the β₂-agonist, and higher doses of the β₂-agonist prevented the subsequent fall in serum gastrin after the initial peak value. This pattern was also found for the histamine H₂-blocker Cimetidine in a dose that blocks acid output. The β₂-agonist and 2-DG increased pulse rate. It is concluded that β₂-sympathetic stimulation inhibits acid output and gastrin release after insulin and 2-DG stimulation, but one should be cautions in drawing conclusions from the insulin experiments. The effect on gastrin release is small compared with the effect on the acid secretion, and it is unlikely that the inhibition of acid secretion acts through a change in gastrin release.

Key-words:

• 2-DG
• dog
• food
• gastric secretion
• gastrin
• insulin
• sympathomimetic