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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 16 (1985), S. 155-159 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The relationship between rat peritoneal mast cell activation and inactivation (desensitization) was studied for a variety of stimuli acting via IgE and IgG receptors on the cell surface. Anti-IgE, antigen (ovalbumin), anti-IgG1, anti-IgG2a and dimers, trimers and higher oligomers of IgE were used to induce histamine release from rat mast cells. All produced similar characteristics of cell activation, with a rapid rate of histamine release from the cells, release being 90% complete within 5 minutes and with calculated doubling times between 21.6±3.6 s (±SEM) for ovalbumin and 93.0±18.6 s (±SEM) for anti-IgG1. The characteristics of inactivation, however, varied with the releasing agent used. Of all the stimuli used only ovalbumin showed a rapid rate of desensitization (t 1/2=330±34.8 s) which correlated with the cessation of histamine release. The other stimuli showed slow rates of desensitization (t 1/2 between 1068±40.2 s for dimer and 3576±660 s for anti-IgE) even though the rate of release was rapid. Thus, although these stimuli are thought to be stimulating the cells by cross-linking of either IgE or IgG receptors, the difference in subsequent response of the cells would indicate that the transduction mechanism bringing about release can distinguish between these various stimuli. Also, it seems that the idea that duration of histamine release is determined by the rate of desensitization may need revising as with most of these stimuli, release has terminated when the cells are still in a fully activated state.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Allergy 42 (1987), S. 0 
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 331 (1985), S. 364-368 
    ISSN: 1432-1912
    Keywords: Substance P ; Somatostatin ; Vasoactive intestinal polypeptide ; Human skin ; Mast cells ; Compound 48/80
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1) Substance P (SP), somatostatin (Som), and vasoactive intestinal polypeptide (VIP) induced a concentration-dependent release of histamine from isolated rat peritoneal mast cells. 2) The release of histamine induced by these neuropeptides was inhibited by preincubation of the cells with the SP analogue [d-Pro4,d-Trp7,9,10]-SP4–11 (SP-A) (10 μM), and also by benzalkonium chloride (10 μM). In addition, SP-A inhibited histamine release induced by compound 48/80, whilst that induced by goat anti-(rat-IgE) was unaffected. 3) In human skin, intradermal injection of SP, Som, or VIP produced flare and wheal responses. The flares to all three peptides were inhibited by preinjection of the skin with SP-A (25 pmol), whilst the wheal responses were unaffected. 4) It is concluded that the receptors mediating histamine release and the flare response are similar, and that SP, Som, and VIP are acting at a similar receptor to produce these effects. It is probable that this receptor is also the site of action of compound 48/80.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 18 (1986), S. 77-80 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The phorbol ester 12-O-tetradecanoyl-13-acetate (TPA) induced a dose-dependent release of histamine from rat peritoneal mast cells at concentrations from 3 to 100 ng/ml. The release is biphasic: an early phase being complete in 15 min and being followed by a second phase extending for more than 50 min. Concentrations of TPA greater than 100 ng/ml produced decreasing releases of histamine. Synergistic interaction in the induction of histamine secretion was observed between TPA and A23187 and between TPA and anti-IgE. Such synergism with anti-IgE was only manifest at low concentrations of TPA and with incubations of the cells with TPA for 5 mins or less. At higher concentrations of TPA and longer incubations, TPA inhibited the response of rat peritoneal mast cells to anti-IgE stimulation. Synergism between A23187 and TPA was observed only at low levels of histamine release induced by calcium plus A23187: at higher levels of release TPA was inhibitory.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Betahistine produced a concentration-dependent contraction of the guinea-pig ileum and was about 27 times less active than histamine in this respect. Betahistine induced desensitization of contractile responses to histamine in the guinea-pig ileum. The H1 histamine receptor antagonist mepyramine was a competitive antagonist of the action of betahistine on the guinea-pig ileum. Betahistine caused relaxation of the rat uterus contracted by acetylcholine, and this action of betahistine was blocked by the H2 receptor antagonist cimetidine. Betahistine had a concentration-dependent positive chronotropic action on isolated guinea-pig atria, and in this respect was tenfold less potent than histamine. The action of betahistine on the atria was blocked by the H2 receptor antagonist YM11170. Betahistine caused a concentration-related contraction of the isolated lung parenchymal strip of the guinea-pig, and YM11170 potentiated this effect. Betahistine failed to release histamine from rat peritoneal mast cells at concentrations up to 100 μM and it did not prevent histamine release induced by either substance P or anti-IgE. Betahistine produced a dose-related flare and wheal reaction when injected intradermally into human skin. It is concluded that betahistine has agonist activity at both H1 and H2 receptors for histamine.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 23 (1988), S. 214-216 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rat peritoneal mast cells were pretreated for 10 min at 37°C with either substance P (SP, 3 or 6 μM) or compound 48/80 (37.5, 50 or 75 ng/ml). The effect of this pretreatment on the subsequent responsiveness of the cells to SP was studied. Both SP and compound 48/80 pretreatment of rat peritoneal mast cells inhibited the subsequent response of the cells to SP. The degree of inhibition produced by either SP or compound 48/80 was dependent on the concentration used to pretreat the cells. Inhibition of the response of the cells to SP was observed whether or not the pretreating agent was removed or remained in contact with the cells during the subsequent stimulation with SP. It is concluded that compound 48/80 and SP desensitize the cells to subsequent stimulation by SP and possible mechanisms for this are discussed.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 20 (1987), S. 165-168 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The phorbol ester 12-O-tetradecanoylphorbol-13-acetate (TPA) and the synthetic diacylglycerol, 1-oleoyl-2-acetylglycerol (OAG) were employed to investigate the consequences of protein kinase C activation in rat peritoneal mast cells. TPA (10 ng/ml) induced a biphasic release of histamine from mast cells. At short periods of incubation histamine release was low; about 10% at 10 min. At 15 min a second phase of release commenced, achieving a maximum at 90 min incubation by which time about 70% of cell histamine was released. Histamine release by TPA was dependent on glycolytic and oxidative metabolism, temperature-dependent and occurred in purified mast cells. In contrast, histamine release induced by OAG 50 μg/ml was maximal after 20 min. Studies usign RHC 80267, a diacylglycerol (DAG) lipase inhibitor, indicated that metabolism of OAG by DAG lipase as well as spontaneous degradation accounts for the comparatively short-lived response to OAG.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 20 (1987), S. 178-180 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The ability of the SP fragments SP2–11 and SP3–11 to release histamine from rat peritoneal mast cells has been compared with that of the whole peptide. SP1–11 was found to be about 3.4 times more active than SP2–11 and about 10.4 times more active than SP3–11. The substance P antagonist [D-Pro4, D-Trp7,9,10] SP4–11 was equally effective at antagonizing the histamine releasing action of SP1–11, SP2–11 and SP3–11. Benzalkonium chloride was found to be a competitive antagonist of SP and SP3–11: the dissociation constants for the benzalkonium chloride-receptor interaction being about the same when either SP1–11 or SP3–11 was used as the agonist.
    Type of Medium: Electronic Resource
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