Potassium-induced histamine release from mast cells and its inhibition by ketotifen

Németh, Á.; Magyar, P.; Herceg, R.; Huszti, Z.

doi:10.1007/bf02074654

Cited by 17 publications

(14 citation statements)

References 6 publications

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“…On the other hand, ketotifen is one of the second-generation antihistamine drugs that exert anti-allergic effects primarily by antagonizing histamine H1 receptors [2]. However, later studies using human conjunctival mast cells additionally revealed a mast cell-stabilizing property of ketotifen [7,8], consistent with its higher potency in the treatment of allergic disorders. So far, by measuring the amount of chemokines released from rat peritoneal mast cells, such as histamine and β-hexosaminidase, previous studies have suggested the superiority of ketotifen to tranilast in the properties of mast cell stabilization [9][10][11].…”

Section: Introductionmentioning

confidence: 96%

“…According to previous in vivo studies, the serum concentration of ketotifen ranges from 10 to 100 nM in humans when orally administered for the treatment of systemic allergic reactions [33,34]. However, in in vitro studies using rat peritoneal mast cells or human conjunctival mast cells, doses as high as 100 µM ketotifen were required to effectively elicit its inhibitory property on histamine release [7,8,35]. Since doses more than 1 mM were cytotoxic enough to cause membrane lysis [36], we tried doses starting from 1 µM up to 100 µM in the present study (Fig.…”

Section: Effects Of Tranilast and Ketotifen On Degranulation From Ratmentioning

confidence: 99%

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Anti-Allergic Drugs Tranilast and Ketotifen Dose-Dependently Exert Mast Cell-Stabilizing Properties

Baba

Tachi²,

Ejima³

et al. 2016

Cell Physiol Biochem

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Background: Anti-allergic drugs, such as tranilast and ketotifen, inhibit the release of chemokines from mast cells. However, we know little about their direct effects on the exocytotic process of mast cells. Since exocytosis in mast cells can be monitored electrophysiologically by changes in the whole-cell membrane capacitance (Cm), the absence of such changes by these drugs indicates their mast cell-stabilizing properties. Methods: Employing the standard patch-clamp whole-cell recording technique in rat peritoneal mast cells, we examined the effects of tranilast and ketotifen on the Cm during exocytosis. Using confocal imaging of a water-soluble fluorescent dye, lucifer yellow, we also examined their effects on the deformation of the plasma membrane. Results: Relatively lower concentrations of tranilast (100, 250 µM) and ketotifen (1, 10 µM) did not significantly affect the GTP-γ-S-induced increase in the Cm. However, higher concentrations of tranilast (500 µM, 1 mM) and ketotifen (50, 100 µM) almost totally suppressed the increase in the Cm, and washed out the trapping of the dye on the surface of the mast cells. Compared to tranilast, ketotifen required much lower doses to similarly inhibit the degranulation of mast cells or the increase in the Cm. Conclusions: This study provides electrophysiological evidence for the first time that tranilast and ketotifen dose-dependently inhibit the process of exocytosis, and that ketotifen is more potent than tranilast in stabilizing mast cells. The mast cell-stabilizing properties of these drugs may be attributed to their ability to counteract the plasma membrane deformation in degranulating mast cells.

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Section: Introductionmentioning

confidence: 96%

Section: Effects Of Tranilast and Ketotifen On Degranulation From Ratmentioning

confidence: 99%

Anti-Allergic Drugs Tranilast and Ketotifen Dose-Dependently Exert Mast Cell-Stabilizing Properties

Baba

Tachi²,

Ejima³

et al. 2016

Cell Physiol Biochem

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“…Sneezing and rhinorrhea could be associated [40,41]. Severe dyspnea and upper airway obstruction may be caused by stings to the face [42][43][44][45][46].…”

Section: Local Symptomsmentioning

confidence: 99%

Jellyfish Envenomation with Skin and Cardiovascular Manifestations and Treatments

Bais¹,

Che²,

Jiang³

et al. 2017

Toxicol Open Access

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Jellyfish are smooth-formed animals in the phylum cnidaria, living in around coastal water zones worldwide. Interacting with jellyfish tentacles, even the beached and dying jellyfish, can prompt millions of nematocysts to perforate the skin and infuse the venom through the inverted long spiny tubules, thereby causing toxic manifestations from no effect to extreme pain to death. According to the structure of nematocyst, quantitative toxins are released into body in a short time. Stung by jellyfish possesses a wide spectrum of toxic effects especially on skin and cardiovascular toxicities. However, the mechanism of jellyfish venom is not clear. In this review, we focus on Jellyfish toxins, symptoms and treatment after sting in order to reduce treatment time, improve the survival rate for medical providers and to set a reference for follow-up study.

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“…Our previous work showed a dose-dependent release of HA from rat peritoneal mast cells by 50 150 mM KC1 in the absence of extracellular Ca + + and a direct effect of K + on the mast cell membrane and its role in HA secretion have been suggested [1]. In order to obtain more data concerning the mechanism of K+-induced HA release fu mast cells, the effects of TEA and TMA have now been studied.…”

Section: Introductionmentioning

confidence: 95%

“…These compounds appeared to be potentially useful tools for studying the possible existence of K § channels in mast cells and their involvement in K § HA release. Rat peritoneal mast cells were obtained from male CFY rats (200-300 g) by washing the peritoneal cavity with buffered saline (PBS) containing NaC1 154 mM, KC1 2 mM, Na2HPO 4 10 mM, KH2PO 4 5mM, CaC12 lmM and MgC12 1raM as described previously [1]. After complete removal of PBS by centrifugation, cells were incubated in 500 gl of 10 mM HEPES buffer containing 150raM KC1 at 37~ for 10 rain.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of potassium-induced release of histamine from mast cells by tetraethylammonium and tetramethylammonium

1990

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In accordance with our previous results, a marked release of histamine (HA) from rat peritoneal mast cells was initiated by 150 mM KCl in the absence of extracellular Ca2+. This release could be reduced by 20-60 mM tetraethylammonium (TEA) or tetramethylammonium (TMA), the non-selective K(+)-channel blockers, Ouabain, the general inhibitor of (Na+ + K+) ATP-ase, failed to produce any changes in this release. The action of TEA discriminated between the initiation of HA release evoked by different agents, producing a blockade of the K(+)-induced but not the 48/80-stimulated HA release. In total, these data suggest the presence of TEA/TMA-sensitive K(+)-channels in the mast cell membrane and their involvement in one of the possible pathways for the initiation of HA release.

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Potassium-induced histamine release from mast cells and its inhibition by ketotifen

Cited by 17 publications

References 6 publications

Anti-Allergic Drugs Tranilast and Ketotifen Dose-Dependently Exert Mast Cell-Stabilizing Properties

Anti-Allergic Drugs Tranilast and Ketotifen Dose-Dependently Exert Mast Cell-Stabilizing Properties

Jellyfish Envenomation with Skin and Cardiovascular Manifestations and Treatments

Inhibition of potassium-induced release of histamine from mast cells by tetraethylammonium and tetramethylammonium

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