Effect of 4-Bromo-3-hydroxybenzyloxyamine (Brocresine) on Gastric Secretion in Pouch Dogs

Tl, Fletcher; Cl, Pitts; Mt, Everett; Ca, Griffith

doi:10.3181/00379727-132-34181

Cited by 6 publications

(2 citation statements)

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“…Kahlson, Rosengren, Svahn & Thunberg (1964) inhibited histidine decarboxylase actity by subjecting rats to semicarbazide superimposed on a pyridoxine-deficient diet without being able to demonstrate any inhibition of gastric secretion. These experiments have been repeated by other workers using other inhibitors of histidine decarboxylase (Levine, 1965;Thayer & Martin, 1967;Lloyd Fletcher, Pitts, Everett & Griffith, 1969) or inhibitors of protein synthesis (Yeh & Shils, 1969;Henman, 1972) since it is known that gastrin-induced increase in histidine decarboxylase activity depends on intact protein synthesis (Snyder & Epps, 1968). Experiments so far with enzyme inhibition have not elucidated this problem.…”

Section: Discussionmentioning

confidence: 99%

Implication of Gastric Mucosal Histamine in Inhibition by Isoprenaline of Pentagastrin‐induced Gastric Secretion

Lundell

Svensson

1974

British J Pharmacology

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The effect of isoprenaline on pentagastrin‐induced gastric secretion was studied in conscious rats with Heidenhain pouches. The influence of isoprenaline on pentagastrin‐induced release and formation of gastric mucosal histamine was also examined. Isoprenaline strongly inhibited pentagastrin‐induced acid secretion, an inhibition which could not be overcome by increasing the dose of pentagastrin. Propranolol blocked the inhibitory effect of isoprenaline on pentagastrin‐induced acid secretion. Isoprenaline enhanced pepsin secretion induced by pentagastrin, an effect which was blocked by propranolol. Isoprenaline reduced the increase in formation and release of gastric mucosal histamine following pentagastrin infusion, an inhibitory influence which was almost completely blocked by propranolol. The inhibition by isoprenaline of pentagastrin‐induced acid secretion is tentatively related to alterations in gastric mucosal histamine occurring simultaneously.

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Section: Discussionmentioning

confidence: 99%

Implication of Gastric Mucosal Histamine in Inhibition by Isoprenaline of Pentagastrin‐induced Gastric Secretion

Lundell

Svensson

1974

British J Pharmacology

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“…In a more detailed study by Fletcher et al (28) neither acute nor chronic administration of NSD 1055 gave rise to any consistent changes in the gastric secretion of canine Pavlov or Heidenhain pouches stimu lated with histamine, gastrin, pentagastrin, or a meal. Jamieson (65) found that the gastric secretory responses of Pavlov pouch dogs to a meat meal or histamine were unaltered following chronic oral or intravenous treatment with 'maximal doses of NSD 1055'.…”

Section: Gastric Secretory Effects O F Decarboxylase Inhibitorsmentioning

confidence: 99%

Amino Acid Decarboxylase Enzymes – Vital or Irrelevant to Gastric Secretion?

Henman¹

1975

Digestion

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The location and discovery of histidine decarboxylase and aromatic L-amino acid decarboxylase in the stomach are described. Feeding and gastrin-like agents stimulate increased gastric histidine decarboxylase (HD) activity in rats. Procedures which result in increased gastrin release – often by raising antral pH – also have this action in intact but not in antrectomised rats. Evidence for a histaminic feedback mechanism controlling HD levels is discussed. HD activity is reduced by protein synthesis inhibitors and by chronic pyridoxine deficiency. The effects of inhibitors of HD on gastric secretion in rat, dog and man are reviewed. The role of HD and histamine in gastric secretion is considered.

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