Effects of pentagastrin and carbachol on the gastric histamine level in ?-fluoromethylhistidine-treated mice and rats

Koyama, Shigeki; Oishi, Ryozo; Saeki, Kiyomi

doi:10.1007/bf00164870

Cited by 9 publications

(3 citation statements)

References 17 publications

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“…Choline esters, such as acetylcholine and carbachol, have been claimed to mobilize histamine from rat and dog stomachs (Stubrin et al ., 1965; Sandvik et al ., 1988c; Gerber & Payne, 1992). On the other hand, there are reports demonstrating a lack of effect of choline esters on ECL‐cell histamine mobilization (Rosengren & Svensson, 1969; Sewing, 1969; Koyama et al ., 1987; Lindström et al ., 1997; Sandvik et al ., 1998; Lindström & Håkanson, 2001). In fact, in the present study, neither of the two choline esters stimulated histamine mobilization in vivo , nor did they inhibit gastrin‐stimulated histamine release.…”

Section: Discussionmentioning

confidence: 99%

ECL‐cell histamine mobilization in conscious rats: effects of locally applied regulatory peptides, candidate neurotransmitters and inflammatory mediators

Norlén

Bernsand

Konagaya

et al. 2001

British J Pharmacology

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1 The ECL cells control gastric acid secretion by mobilizing histamine in response to circulating gastrin. In addition, the ECL cells are thought to operate under nervous control and to be in¯uenced by local in¯ammatory processes. 2 The purpose of the present study was to monitor histamine mobilization from ECL cells in conscious rats in response to locally applied regulatory peptides, candidate neurotransmitters and in¯ammatory mediators. 3 Microdialysis probes were implanted in the submucosa of the acid-producing part of the rat stomach. Three days later, the agents to be tested were administered via the microdialysis probe and their eects on basal (48 h fast) and stimulated (intravenous infusion of gastrin-17, 3 nmol kg 71 h 71 ) mobilization of ECL-cell histamine was monitored by continuous measurement of histamine in the perfusate (radioimmunoassay). 4 Locally administered gastrin-17 and sulfated cholecystokinin-8 mobilized histamine as did pituitary adenylate cyclase-activating peptide-27, vasoactive intestinal peptide, peptide YY, metenkephalin, endothelin and noradrenaline, adrenaline and isoprenaline. 5 While gastrin, sulfated-cholecystokinin-8, met-enkephalin and isoprenaline induced a sustained elevation of the submucosal histamine concentration, endothelin, peptide YY, pituitary adenylate cyclase activating peptide, vasoactive intestinal peptide, noradrenaline and adrenaline induced a transient elevation. 6 Calcitonin gene-related peptide, galanin, somatostatin and the prostanoid misoprostol inhibited gastrin-stimulated histamine mobilization. 7 The gut hormones neurotensin and secretin and the neuropeptides gastrin-releasing peptide, neuropeptide Y and substance P failed to aect ECL-cell histamine mobilization, while motilin and neuromedin U-25 had weak stimulatory eects. Also acetylcholine, carbachol, serotonin and the amino acid neurotransmitters aspartate, g-aminobutyric acid, glutamate and glycine were inactive or weakly active as was bradykinin. 8 In summary, a range of circulating hormones, local hormones, catecholamines, neuropeptides and in¯ammatory mediators participate in controlling the activity of rat stomach ECL cells in situ.

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Section: Discussionmentioning

confidence: 99%

ECL‐cell histamine mobilization in conscious rats: effects of locally applied regulatory peptides, candidate neurotransmitters and inflammatory mediators

Norlén

Bernsand

Konagaya

et al. 2001

British J Pharmacology

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“…tt-Fluoromethylhistidine (a-FMH) covalently binds to histidine decarboxylase (HDC) and irreversibly inhibits enzyme activity with consequent decrease in histamine synthesis and acid secretion [45,46], Andersson et al [47,48] utilized a-FMH as a probe to evaluate ECL cell proliferation and histamine production. They inter preted that ECL cell histamine was not important for a full expression of gastrin-evoked trophic effects in the stomach.…”

Section: Discussionmentioning

confidence: 99%

Evidence for a Regulatory Role for Histamine in Gastric Enterochromaffin-Like Cell Proliferation Induced by Hypergastrinemia

Modlin

Zhu²,

Tang³

et al. 1996

Digestion

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Background/Aims: Hypergastrinemia, induced by sustained suppression of gastric acid secretion, is associated with gastric enterochromaffin-like (ECL) cell hyperplasia and carcinoid tumor formation. We examined the effect of a selective Hi-histamine antagonist, terfenadine, on gastric mucosal cell proliferation to determine whether histamine might modulate ECL cell generation. Methods: The rodent mastomys received the H₂-antagonist loxtidine (2 g/l drinking water) alone or in combination with terfenadine (0.5 g/l or 35 mg/l drinking water) for 120 days. Controls received water or terfenadine alone. Serum gastrin levels and tissue histamine content were assayed by radioimmu-noassays, and tissue chromogranin levels determined (Western blot analysis). In vivo cell proliferation was measured by bromodeoxyuridine (BrdU, 200 mg/kg/day, 3 days) incorporation. Gastric mucosal thickness was determined, ECL cell number was assessed, and the percentage of proliferating ECL cells quantitated. To evaluate the direct action on ECL cells we then studied the effect of terfenadine on histamine secretion and DNA synthesis (BrdU uptake) in an isolated preparation (∼ 90% pure) of ECL cells. Results: Loxtidine increased serum gastrin levels, mucosal thickness, tissue chromogranin levels, tissue histamine content, BrdU incorporation, ECL cell number, and proliferating ECL cells (all parameters p < 0.05). Terfenadine alone, irrespective of dosage, had no significant effect. The high dose in combination with loxtidine significantly inhibited the increase in tissue chromogranin levels, tissue histamine content, ECL cell number and proliferating ECL cells (p < 0.05), but did not alter other parameters, compared to loxtidine alone. The low dose did not alter the loxtidine-induced changes. In pure isolated ECL cells, terfenadine did not alter histamine secretion either alone or in combination with gastrin (10 nM). DNA synthesis was significantly inhibited by terfenadine (IC₅₀ 10^-10M). Conclusions: Terfenadine specifically inhibited the effect of loxtidine-induced ECL cell proliferation in vivo and significantly inhibited ECL cell DNA synthesis in vitro. We postulate that histamine, through an H₁ receptor, positively modulates gastric ECL cell proliferation.

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“…Brocresine (NSD-1055) has been used as an inhibitor of HDC, but was found to lack selectivity [7], Another compound, afluoromethylhistidine (a-FMH), has been shown to be a more potent and specific inhibitor of HDC [8]. This compound has been used in the rat for in vivo inhibition of histamine formation [9][10][11].…”

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confidence: 99%

The Role of Gastric Mucosal Histamine in Acid Secretion and Experimentally Induced Lesions in the Rat

Andersson¹,

Mattsson²,

Larsson³

1990

Digestion

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The role played by histamine from enterochromaffin-like (ECL) cells and mast cells in gastric acid secretion and in the development of ethanol-induced gastric lesions was studied in the rat. This was done by examining the effects of inhibition of the histamine-producing enzyme histidine decarboxylase (HDC) with α-fluoromethylhistidine (α-FMH) and the effects of degranulation of the mucosal mast cells with dexamethasone. A single dose of α-FMH (50 mg/kg p.o.) inhibited the HDC activity by 94% but did not affect histamine levels in the gastric mucosa 2 h after dose. Repeated treatment resulted in an almost complete inhibition of HDC activity and in a reduction of histamine levels by 75 %. Pentagastrin failed to stimulate acid secretion after 4 days treatment with α-FMH, whereas the acid response to histamine was unaffected in chronic gastric fistula rats. Ethanol failed to induce gastric lesions in rats pretreated for 4 days with dexamethasone whereas 4 days pretreatment with α-FMH did not influence ethanol-induced lesion formation. The present results show that histamine synthesis is required for pentagastrin-stimulated gastric acid secretion and that mucosal mast-cell histamine plays a role in the development of ethanol-induced gastric lesions.

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Effects of pentagastrin and carbachol on the gastric histamine level in ?-fluoromethylhistidine-treated mice and rats

Cited by 9 publications

References 17 publications

ECL‐cell histamine mobilization in conscious rats: effects of locally applied regulatory peptides, candidate neurotransmitters and inflammatory mediators

ECL‐cell histamine mobilization in conscious rats: effects of locally applied regulatory peptides, candidate neurotransmitters and inflammatory mediators

Evidence for a Regulatory Role for Histamine in Gastric Enterochromaffin-Like Cell Proliferation Induced by Hypergastrinemia

The Role of Gastric Mucosal Histamine in Acid Secretion and Experimentally Induced Lesions in the Rat

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