Inhibition of gastric acid secretion in dogs by a new sympathomimetic drug.
The effect of salmefamol, a new beta 2-agonist, on pentagastrin-induced gastric acid secretion was studied in conscious gastric fistula dogs. Salmefamol inhibited the acid secretion, an effect which was dose dependent. The volume as well as the acidity was inhibited. Salmefamol caused an increase in the pulse rate. Propranolol prevented the inhibition of acid output as well as the increase in pulse rate. Practolol, a beta 1-adrenoceptor blocker, had no effect on the inhibition of acid secretion but prevented the increase in pulse rate. Dose-response experiments with 6 doses of pentagastrin and 1 dose of salmefamol showed a decrease in calculated maximal response (CMR) and an unchanged D50. It is concluded that salmefamol strongly inhibits pentagastrin-induced acid output in the dog, and the inhibition follows a non-competitive kinetic. The mechanism of gastric secretion probably involves a beta 2-receptor.
D000818:Animals; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004983:Ethanolamines / Q000494:pharmacology*; D005260:Female; D005750:Gastric Juice / Q000378:metabolism*; D008297:Male; D010418:Pentagastrin / Q000494:pharmacology; D011217:Practolol / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D012636:Secretory Rate / Q000187:drug effects
D004983:Ethanolamines; D011433:Propranolol; D010418:Pentagastrin; D011217:Practolol