Effect of His-Phe, a competitive inhibitor of histidine decarboxylase, on gastric acid secretion in chronic gastric fistula rats: delay in acid secretion response to pentagastrin.
The dipeptide His-Phe, earlier shown to inhibit mammalian histidine decarboxylase, was analysed concerning its effect in vivo on pentagastrin-induced gastric acid secretion. Chronic gastric fistula rats were used and the effectors in saline were given as continuous i.v. infusions while acid was collected from the fistula. Addition of pentagastrin to the infusion solution resulted in an immediate increase in the acid output of the control runs. In the His-Phe experiments the dipeptide was introduced one hour before pentagastrin. A significant decrease in the acid output was obtained. This effect was optimal at a dose of about 6 mg/h and during the first few hours of the experiments. In spite of the continuous His-Phe infusion the acid secretion increased with time to the control values. These results are discussed in relation to preliminary observations on effects of alpha-fluoromethyl histidine on gastric acid secretion and the effect of this and His-Phe on gastric histamine content and histidine decarboxylase activity.
D000818:Animals; D001667:Binding, Competitive; D002262:Carboxy-Lyases / Q000037:antagonists & inhibitors*; D004151:Dipeptides / Q000494:pharmacology*; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D006640:Histidine Decarboxylase / Q000037:antagonists & inhibitors*; D010418:Pentagastrin / Q000037:antagonists & inhibitors*; D051381:Rats; D011919:Rats, Inbred Strains; D013270:Stomach / Q000502:physiology
D004151:Dipeptides; C022144:histidylphenylalanine; D002262:Carboxy-Lyases; D006640:Histidine Decarboxylase; D010418:Pentagastrin