Non-mast cell histamine levels in rat tissues after histidine loading

Huszti, Z.; Kenessey, Ágnes; Kürti, Marianne

doi:10.1016/0014-2999(77)90289-8

Cited by 11 publications

(7 citation statements)

References 28 publications

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“…Histamine in tissues is believed to derive mostly from decarboxylation of histidine, (see Schayer, 1978), yet injections of histidine do not increase histamine levels in all tissues of mouse and rat containing decarboxylases (Taylor and Snyder, 1972;Schwartz etal., 1972;Huszti et al, 1977;Endo, 1979). This is a surprising finding, for histidine can be decarboxylated by both histidine decarboxylase, i.e., E.C.…”

Section: Metabolism Of Histaminementioning

confidence: 73%

Aspects of histamine metabolism

et al. 1987

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Section: Metabolism Of Histaminementioning

confidence: 73%

Aspects of histamine metabolism

et al. 1987

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“…dose of histidine [7,8]. However, the histamine concentration in the stomach and liver of rats and mice did not increase after histidine loading [7,9].…”

Section: Introductionmentioning

confidence: 89%

“…There is a paucity of data regarding HMT in the local regulation of newly formed histamine. It has recently been suggested [9] that the efflux may be more significant than the forming capacity in the regulation of tissue histamine levels. In this laboratory it was noted that tissue histamine concentrations were apparently not directly regulated through the activities of either the synthesizing or degradative enzymes [10l.…”

Section: Introductionmentioning

confidence: 99%

Effect of age and dietary histidine on histamine metabolism of the growing chick

et al. 1979

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The effect of age and of varying the dietary histidine level, with special emphasis on histamine metabolism, was studied in male, white Leghorn chicks. The birds were fed a 19% amino acid diet with histidine supplied from 0 to 0.8% of dict. In Experiment 1, 7-day-old chicks were fed the experimental diets for 7 days. In Experiment 2, chicks were fed the experimental dlets for different time intervals to equalize their body weight at time of killing. In Experiment 3, blrds were killed at 5, 9, 12 and 15 days of age when their body weights reached 69, 96, 136 and 184 g, respectively. Concentrations of anserine, carnoslne, free-hlstldlne and histamine, and actlvitles of histldine deearboxylase (HDC) and histamine methyl transferase (HMT) were assayed in whole brain, pectoralis major muscle and in proventrlculus of 3 or 4 chicks per treatment group.The following results were obtained: As the level of dietary hlstidlne increased, (1) tissue concentrations of freehistidine and of carnosine increased; (2) the activity of HMT increased; (3) the concentratlon of anserine remained constant; (4) the activity of HDC increased in brain and muscle, but decreased sharply in the proventrieulus; (5) the concentration of histamine decreased. (6) Free-histidine concentration, HDC and HMT activities increased with an increase in age and body weight; however, histamine concentrations decreased with age and body weight. The results point to the possibility that the relatively greater increase in HMT activity compared to HDC may be responsible for the decrease in histamine concentration with increase in dietary histidlne or increased age. The very high HDC activity in the proventrlculus of birds fed low histidine diets may have contributed to the higher histamine concentrations in brain and muscle of blrds fed low versus higher histldine-containing diets.

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“…By similar treatment, the HD activity in the glandular stomach increased linearly with the newly synthesized HA (Table 2). This suggests rapid elimination of the newly synthesized amine from the stomach into the blood [9]. In these rats, the HD activity values were slightly below that of the control values.…”

Section: Tablementioning

confidence: 74%

Induction of gastric histamine synthesis by H2-receptor antagonists: Potentiation of their antisecretory activity by histidine decarboxylase inhibitors

Huszti¹,

Pik

Frenkl

1980

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The activation of histamine (HA) formation in rat stomach was measured after repeated administration of histamine H2-receptor antagonists and the potentiation of their antisecretory activity was examined in histidine decarboxylase inhibitor (HDI)-pretreated rats. 40 mg/kg of metiamide, given intraperitoneally (i.p.) 24, 16 and 2 h prior to the examination, produced approximately 50% increase in the amount of 14C-histamine, formed from 14C-histidine in the stomach, and an almost equal enhancement in the gastric histidine decarboxylase (HD) activity. An equal dose of the compound did not influence the endogenous histamine level in the glandular stomach whereas it caused a significant increase in the serum histamine content. By similar treatment, 10 mg/kg of cimetidine enhanced the newly formed histamine in the rat stomach by 57%. The potent HDI, 2-hydroxy-5-carbomethoxy-benzyloxyamine (GYKI-11 121) suppressed the metiamide- and cimetidine-induced increases in histamine synthesis to slightly above or below the control values. In pharmacological studies, the antisecretory activity of histamine H2-receptor blockers could markedly be potentiated by HDI. In GYKI-11 121 and NSD-1055-pretreated rats, the inhibiting potency of metiamide and cimetidine on pentagastrin-stimulated gastric acid secretion, increased to approximately twice that of the original effect. Neither GYKI-11 121 nor NSD-1055 produced significant inhibition on pentagastrin-stimulated gastric acid secretion in the applied doses. These findings provided evidence for the feedback stimulation of gastric HA synthesis by H2-receptor blockers and confirmed the role of HA in the gastric acid secretion. Potentiation of the antisecretory activity of H2-receptor antagonists by HDI would be useful in the therapeutic application of these compounds.

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Non-mast cell histamine levels in rat tissues after histidine loading

Cited by 11 publications

References 28 publications

Aspects of histamine metabolism

Aspects of histamine metabolism

Effect of age and dietary histidine on histamine metabolism of the growing chick

Induction of gastric histamine synthesis by H2-receptor antagonists: Potentiation of their antisecretory activity by histidine decarboxylase inhibitors

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