Gastrin: obligatory intermediate for activation of gastric histidine decarboxylase in the rat

Aures, D.; Johnson, L. R.; Way, LW

doi:10.1152/ajplegacy.1970.219.1.214

Cited by 34 publications

(17 citation statements)

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“…These results are at variance with reports by Johnson, Jones, Aures & Hakanson (1969) and Aures, Johnson & Way (1970), who failed to demonstrate any mucosal histidine decarboxylase activity after antrectomy, while others have reported an unaltered enzymic activity (Hikanson & Liedberg, 1970. After antrectomy the responsiveness of the enzyme to injected HISTAMINE METABOLISM AFTER ANTRECTOMY 449 pentagastrin has been reported as unaltered Aures et al 1970) or even increased (HAkanson & Liedberg, 1972).…”

Section: Discussioncontrasting

confidence: 78%

Histamine metabolism of the gastric mucosa following antrectomy

Lundell¹

1974

The Journal of Physiology

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SUMMARY1. Histamine metabolism of the gastric mucosa in rats subjected to antrectomy, antrectomy and substitution with pentagastrin and exclusion of the antrum has been investigated employing various in vivo and in vitro methods.2. Mucosal histamine formation after antrectomy fell to about one third, whereas after antrum exclusion histamine formation increased many-fold.3. After antrectomy, mucosal histamine content decreased, and increased after antrum exclusion.4. After total gastrectomy, (a) whole-body histamine formation was reduced to about half, as judged by determining histamine excretion, and (b) pentagastrin infusion did not increase histamine excretion, showing absence of histamine mobilization from extra-gastric sources. In rats with the stomach retained, infusion of pentagastrin induced a dose-dependent increase in histamine excretion.5. Kinetic studies in which [14C]histidine was injected and the resulting urinary [14C]histamine determined showed that on pentagastrin infusion after antrectomy newly formed histamine was initially mobilized to a larger extent than in the controls.6. Antrectomized rats were subjected to substitution treatment by three injections per day of pentagastrin. After 3 weeks of substitution, histamine excretion was considerably higher than without substitution. After 6 weeks of substitution, histamine excretion was about the same in the substituted antrectomized, non-substituted antrectomized and shamoperated groups. Neither time nor substitution could, however, normalize the excretion of histamine on pentagastrin stimulation after antrectomy.7. In non-substituted antrectomized rats, pentagastrin was less effective in elevating mucosal histamine formation than in the substituted and sham-operated groups.8. The indispensability of the rat in this kind of study is emphasized.438

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Section: Discussioncontrasting

confidence: 78%

Histamine metabolism of the gastric mucosa following antrectomy

Lundell¹

1974

The Journal of Physiology

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“…Furthermore, the enzyme-activating effect of various surgical and pharmacological treatments was abolished by antrectomy whereas that of gastrin or gastrin analogues was not (Johnson, Jones, Aures & Hikanson, 1969;Aures, Johnson & Way, 1970;Hakanson & Liedberg, 1970, 197 la, b;HAkanson, Liedberg & Sj6lund, 1972;HAkanson, Liedberg & Oscarson, 1973a; HAkanson, Liedberg, Oscarson, Rehfeld & Stadil, 1973b). This study is concerned with the role of endogenous gastrin in the enzyme activation after H2-receptor blockade.…”

Section: Introductionmentioning

confidence: 99%

ACTIVATION OF HISTIDINE DECARBOXYLASE BY H₂‐RECEPTOR BLOCKADE: MECHANISM OF ACTION

Håkanson

Hedenbro

Liedberg

et al. 1975

British J Pharmacology

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1 Treatment with histamine H 2-receptor antagonists, which inhibit basal acid secretion, was found to activate rat stomach histidine decarboxylase. At the same time the serum gastrin concentration was greatly increased. 2 In antrectomized rats neither the enzyme activity nor the serum gastrin concentration was affected by the treatment. 3 In analogy with pr,,vious observations on other inhibitors of acid secretion we suggest that the H 2-receptor antagonists stimulate gastrin release through their effect on acid secretion and that the raised serum gastrin level is responsible for the enzyme activation.

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“…Gastrin (8,67,76,125,131) and molecules containing the active C-terminal tetrapeptide of gastrin, such as pentagastrin (8,9,42,72,154,155) caerulein (107), cholecystokinin (CCK) (8), and the C-terminal heptapeptide of CCK (107) have been shown to stimulate increased gastric histidine decarboxylase activity in the rat. Drugs which cause gastric secretion by stimulating, or by mimicking the stimulation of, the vagus nerve such as insulin (8,38,79,131), 2-deoxy-D-glucose (2-DG) (8,79,131), bethanechol (urecholine) (3,8) and carbachol (38,115) also increase gastric histidine decarboxylase activity in the rat.…”

Section: Physiological and Pharmacological Regulation O F Enzyme Levelsmentioning

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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Gastrin: obligatory intermediate for activation of gastric histidine decarboxylase in the rat

Cited by 34 publications

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Histamine metabolism of the gastric mucosa following antrectomy

Histamine metabolism of the gastric mucosa following antrectomy

ACTIVATION OF HISTIDINE DECARBOXYLASE BY H₂‐RECEPTOR BLOCKADE: MECHANISM OF ACTION

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

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Gastrin: obligatory intermediate for activation of gastric histidine decarboxylase in the rat

Cited by 34 publications

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Histamine metabolism of the gastric mucosa following antrectomy

Histamine metabolism of the gastric mucosa following antrectomy

ACTIVATION OF HISTIDINE DECARBOXYLASE BY H2‐RECEPTOR BLOCKADE: MECHANISM OF ACTION

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

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ACTIVATION OF HISTIDINE DECARBOXYLASE BY H₂‐RECEPTOR BLOCKADE: MECHANISM OF ACTION