Effect of a beta 2-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.

The effect of a selective beta 2-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 beta 2-sympathetic infusion, whereas a slight increase in blood and glucose was found. The beta 2-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 beta 2 infusion. After feeding, gastrin release was initially decreased for one of five doses of the beta 2-agonist, and higher doses of the beta 2-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 beta 2-agonist and 2-DG increased pulse rate. It is concluded that beta 2-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.