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1.
The calcium antagonists verapamil and nifedipine inhibited histamine release induced from rat peritoneal mast cells by a number of secretory stimuli. However, the concentrations required were much higher than those active in smooth muscle preparations. The inhibition was unaffected by elevated levels of external calcium and the drugs prevented release in the absence of added calcium. The novel calcium antagonist, PY 108-068, had no effect on histamine secretion from mast cells. These results suggest that calcium channels in the mastocyte may differ from those in smooth muscle and that at concentrations required to inhibit secretion, verapamil and nifedipine may have non-specific stabilizing effects on the mast cell membrane. 相似文献
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Inflammation Research - 相似文献
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Summary The present communication endeavours to elucidate the mechanism of histamine release from rat peritoneal mast cells induced by selective histamine liberators.Of the different enzymatic processes involved in secretion the following are considered: ecto-ATPase activity in the mast cell, pro-esterase-esterase conversion during histamine secretion, cyclic AMP and microtubule association/dissociation, phospholipase A2 and the effect of phospholipid metabolites on secretion, N-methyl transferase and the methylation of phospholipids and the phosphorylation and desphosphorylation of proteins. 相似文献
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B. UVNS C. -H. BORG L. LYSSARIDES L. G. DANIELSSON 《Acta physiologica (Oxford, England)》1991,142(2):173-180
Isolated rat peritoneal mast cells release histamine when superfused with isoosmotic salt or sucrose solutions. The release was ascribed by us to an intracellular ion exchange between potassium and histamine at granule sites, resulting from a flux of cytoplasmic potassium across the granules secondary to the disturbance of the ‘state of equilibrium’ at the cell surface caused by the superfusion (Uvnäs et al. 1989). In the present article is shown that the histamine releasing effect is counteracted by the addition of histamine to the superfusion fluid. The inhibition is concentration-dependent and accompanied by concomitant changes in the potassium efflux. A 50% inhibition of the histamine release requires an external histamine concentration of 40 μm and extrapolation of the equilibrium curve hints at a total inhibition at concentrations around 170 μm. The observations are taken to indicate that reduction of the juxtacellular histamine concentration caused by the superfusion disturbs the histamine equilibrium at the mast cell surface resulting in the activation of the histamine secretory mechanism. In other words, the secretory activity of the mast cell is checked by the juxtacellular concentration of histamine. When the juxtacellular histamine is removed e.g. on isolation procedures, other experimental situations such as superfusion, or by consumption in vivo the mast cell delivers histamine to restore the juxtacellular equilibrium. 相似文献
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Canatoxin, a toxic protein present in the seeds ofCanavalia ensiformis, induces the secretion of serotonin, dopamine and insulin through activation of the lipoxygenase pathway. The purpose of the present study was to verify if canatoxin causes histamine release from rat peritoneal mast cells and to perform a detailed study of this phenomenon. Our results indicate that canatoxin is capable of activating mast cells to release histamine. The process is time- and concentration-dependent, occurs without cell damage and requires metabolic energy as well as the presence of divalent cations (Ca2+ and Mg2+). Optimal release occurs at 37°C and at physiological pH. Extremes of temperature (0°C and 45°C) inhibit the process. We conclude that canatoxin induces histamine release from rat peritoneal mast cells by an active secretory process. 相似文献
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Purified rat peritoneal mast cells rapidly accumulated45calcium from the external medium. The uptake was essentially unaffected by lanthanide ions but was almost totally prevented by metabolic inhibitors. Cells preloaded with45calcium showed a steady efflux of the cation on transfer to a medium lacking the isotope. The efflux was unaffected by metabolic inhibitors but was totally dependent on extracellular sodium ions. These results indicate the operation of a sodium-calcium exchange mechanism for the extrusion of the divalent cation. Antigenic or pharmacologic stimulation of the mast cell led to a temporary suppression of calcium efflux during the period in which histamine release occurred. This effect was potentiated by phosphatidylserine and high concentrations of the lipid inhibited basal efflux. These results suggest that activation of the mast cell leads to an inhibition of calcium extrusion, thereby potentiating the induced rise in the intracellular concentration of the cation and thus augmenting the secretory response. 相似文献
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The production of five prostanoids (PGD2, PGE2, PGF2, 6-oxo-PGF1, and TxB2) was examined after mast cell activation. Prostaglandin D2 (PGD2) was the major prostanoid produced after stimulation of rat peritoneal mast cells with the calcium ionophore A 23187, compound 48/80 or anti-rat IgE. The amount of PGD2 generated was not dependent on the quantity of histamine released. The time course of PGD2 production paralleled the release of histamine following activation with A 23187 or anti-rat IgE but with compound 48/80 release of histamine reached a maximum within 15 sec, whereas production of PGD2 was apparent only after 5 min and was still increasing at 30 min. 相似文献
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Dantrolene strongly and dose-dependently inhibited histamine release from rat peritoneal mast cells induced by anti-IgE. Dantrolene inhibited Ca2+-mobilization from intracellular Ca2+-store as well as histamine release in mast cells activated by anti-IgE, the effect on both of these phenomena being closely correlated. These results suggested that the effect of dantrolene on histamine release from rat mast cell might be due to the inhibition of Ca2+-release from intracellular Ca2+-store. 相似文献
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Isolated rat peritoneal mast cells release histamine when superfused with isoosmotic salt or sucrose solutions. The release was ascribed by us to an intracellular ion exchange between potassium and histamine at granule sites, resulting from a flux of cytoplasmic potassium across the granules secondary to the disturbance of the 'state of equilibrium' at the cell surface caused by the superfusion (Uvn?s et al. 1989). In the present article is shown that the histamine releasing effect is counteracted by the addition of histamine to the superfusion fluid. The inhibition is concentration-dependent and accompanied by concomitant changes in the potassium efflux. A 50% inhibition of the histamine release requires an external histamine concentration of 40 microM and extrapolation of the equilibrium curve hints at a total inhibition at concentrations around 170 microM. The observations are taken to indicate that reduction of the juxtacellular histamine concentration caused by the superfusion disturbs the histamine equilibrium at the mast cell surface resulting in the activation of the histamine secretory mechanism. In other words, the secretory activity of the mast cell is checked by the juxtacellular concentration of histamine. When the juxtacellular histamine is removed e.g. on isolation procedures, other experimental situations such as superfusion, or by consumption in vivo the mast cell delivers histamine to restore the juxtacellular equilibrium. 相似文献
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Yasufumi Horinouchi Kihachiro Abe Keiji Kubo Masuichiro Oka 《Inflammation research》1993,40(1-2):28-36
The mechanisms of vancomycin (VCM)-induced histamine release were studied with rat peritoneal mast cells. VCM (>1×10–3
M) released histamine from the isolated mast cells in a dose-dependent and noncytotoxic manner. In the absence of extracellular Ca2+, the histamine release was reduced markedly. When the intracellular Ca2+ was depleted, it was further decreased. The Fura-2-loaded single mast cells showed a biphasic increase in the intracellular Ca2+ concentration ([Ca2+]i) by VCM: the first transient and the second sustained components. In the absence of extracellular Ca2+, the transient component was unchanged, while the sustained component was eliminated completely. The IP3 content in the mast cells increased within 10 s after the application of VCM. These results suggest that VCM releases histamine from rat peritoneal mast cells via an IP3 production and increase in [Ca2+]i. 相似文献
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The effect of auranofin on histamine release from immunologic and non-immunologic activated rat peritoneal mast cells cocultured with 3T3 fibroblasts (MC/3T3) was investigated. When MC/3T3 were preincubated with 2 x 10(-5) M auranofin and thereafter challenged with anti-IgE antibodies, a maximal inhibition of histamine release (86.2%) was obtained. Non-immunological histamine release induced by compound 48/80, substance P and bradykinin was inhibited to a lesser degree, i.e. 36.0%, 37.6% and 24.0% respectively. Simultaneous incubation of auranofin and the stimulating agents resulted in a higher inhibition of histamine release: anti-IgE antibodies--92.0%; compound 48/80--73.5%; substance P--46.1%. We conclude that auranofin effectively reduces histamine release from immunologic and non-immunologic activated mast cells. This may be relevant to the control of allergic reactions. 相似文献
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《International journal of immunopharmacology》1984,6(3):233-240
The release of histamine from purified rat peritoneal mast cells induced by specific antigen (egg albumin), compound 48/80 and calcium ionophore A23187 was modified by tartrazine. Histamine release induced by 48/80 and antigen was inhibited by the presence of 10−5 to 10−2M tartrazine. The inhibitory effect on egg albumin induced histamine release was maximal when the tartrazine was added simultaneously with egg albumin, and was reduced by increased preincubation of the cells with tartrazine. Tartrazine had a small inhibitory effect on ionophore induced release at high concentrations, but augmented histamine release at tartrazine concentrations of 10−3 and 10−4M. Augmentation of ionophore induced release was maximal at between 0–5 min preincubation of the cells with tartrazine. 相似文献
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Compound 48/80-induced histamine release (HR) from the isolated perfused rat heart was markedly and significantly inhibited by picumast (PIC), possibly by acting as a calmodulin antagonist (CMA) or membrane stabilizer. Trifluoperazine (TFP, another CMA in clinical use) had a similar effect. However, an action as CMA being the basis of inhibition of HR could not be confirmed in another allergy model, namely HR from rat peritoneal mast cells (RPMC). PIC, TFP and two other CMA, W7 andN-(4-aminobutyl)-5-chloro-1-naphthalenesulfonamide) failed consistently to inhibit 48/80-induced HR from RPMC, and when used on their own at high concentration these compounds caused HR. PIC and TFP also potentiated the heat-induced haemolysis of rat erythrocytes, i.e. lacked membrane stabilizing effect in this model. 相似文献
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Objectives and design: The objective of this study was to explore whether increased levels of inflammatory cytokines are associated with the risk
of clinically silent coronary artery disease.
Subjects: Three-hundred-fifty-six black adults aged 25–54 residing in inner city of Baltimore, Maryland, United States were included
in this study.
Methods: Sociodemographics were assessed as were lipid profiles, IL-6, tumor necrosis factor-alpha (TNF-alpha), soluble intercellular
adhesion molecule-1 (sICAM-1), and high-sensitivity C-reactive protein (hs-CRP) levels. Computed tomography (CT) coronary
angiography was performed.
Results: Coronary calcification was identified in 22.5 % participants and 14 % had significant (≥50 %) coronary stenosis. Multiple
logistic regression analyses suggested that IL-6 levels were independently associated with the presence of coronary calcification
and significant coronary stenosis, while TNF-alpha, sICAM-1 and hs-CRP levels were not.
Conclusions: This study underscores a critical role for IL-6 in atherosclerosis and suggests that IL-6 may be a marker for significant
coronary stenosis in cardiovascularly asymptomatic individuals.
This research was funded by National Institute on Drug Abuse grants RO1-DA12777 (Lai S), and RO1-DA15020 (Lai S).
Received 22 November 2007; returned for revision 28 May 2008; received from final revision 6 August 2008; accepted by M. Parnham
7 August 2008 相似文献
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Inflammation Research - 相似文献
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Conclusion It may be concluded that both exogenous cAMP and cGMP exert a certain influence on histamine release from rat peritoneal mast cells. It is probably due to their action on membrane receptors and/or some changes of the intracellular pool of cyclic nucleotides. 相似文献
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Rat peritoneal mast cells were incubated with different concentrations of naturally occurring aliphatic polyamines, spermine and spermidine, at 0.1-10 mM and the amount of histamine release into the supernatant solutions was measured. The addition of each polyamine to the suspensions of the mast cells caused a histamine release in a dose-dependent manner. The effect of 10 mM spermine and spermidine was as much as that of 0.5 microgram/ml compound 48/80. The histamine release from the cells incubated with each polyamine was rapid and the amount of histamine release into the supernatant solutions reached a maximum at 1 min with the incubations. 0.1 mM spermine, which in itself could not cause a significant histamine release, showed a tendency to enhance anti-IgE-induced histamine release from the mast cells. 相似文献