Effect of a beta2-sympathomimetic on urecholine-stimulated gastric acid secretion in dogs.
The effect of a selective beta2-adrenoceptor agonist on urecholine-stimulated gastric acid secretion was studied in conscious gastric fistula dogs. A dose-dependent inhibition was found, most pronounced for the highest doses of urecholine. The inhibition was primarily on volume, whereas the acidity showed a decreasing tendency only. The pulse rate was increased by the beta2-agonist and by urecholine in high doses. Propranolol prevented both the inhibition of acid secretion and the increase in pulse rate. Practolol had no effect on the inhibition of acid secretion and the increase in pulse rate. Practolol had no effect on the inhibition of acid secretion but prevented the increase in pulse rate. Dose-response experiments with five doses of urecholine and two doses of the beta2-agonist showed a decrease in maximal response, and transformation of the curve suggested an unchanged D50. It is concluded that the beta2-agonist inhibits urecholine-stimulated acid secretion in the dog to the same degree as pentagastrin-induced acid secretion, and much stronger than found for histamine-induced acid secretion in earlier experiments. The inhibition seems to follow a noncompetitive kinetic, and beta2-receptors are probable involved.
D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000818:Animals; D001626:Bethanechol Compounds / Q000494:pharmacology*; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004983:Ethanolamines / Q000494:pharmacology; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D008297:Male; D011674:Pulse / Q000187:drug effects; D013268:Stimulation, Chemical
D000318:Adrenergic beta-Agonists; D001626:Bethanechol Compounds; D004983:Ethanolamines; C100251:salmefamol