Mechanism of Bradykinin-Induced Histamine Release from Rat Peritoneal Mast Cells.
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Bradykinin at concentrations higher than 2 microM caused a significant histamine release from rat peritoneal mast cells when extracellular Ca2+ was removed from the medium. Under the same experimental conditions, bradykinin increased Ca2+ release from the intracellular Ca store of the rat peritoneal mast cells, and a clear relationship was observed between the magnitude of histamine release and an increase in fluorescence intensity. Addition of Ca2+ to the medium resulted in an inhibition of the response to bradykinin in a concentration-dependent manner. Almost the same results were obtained when Mg2+, Ba2+ and La3+ were added to the medium. Neither B1 nor B2 antagonists caused significant antagonistic effects on histamine release induced by bradykinin. However, B2 antagonists caused a histamine release of the same potency as bradykinin when applied alone. These results indicate that bradykinin-induced histamine release is not attributable to a bradykinin receptor.Keywords:
Histamine H4 receptor
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Compound 48/80
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Histamine is present in mast cells and non-mast cells, but the relation of physiological roles of histamine to its storage site is not clear. We have studied histamine pharmacology from the viewpoint of its storage cells.
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The purpose of this study was to investigate histamine and skin mast cells in psoriasis before and during 6 months of treatment with high-dose ranitidine. Sixteen psoriasis patients, presenting a mean PASI score of 15.4, were compared with 13 age- and sex-matched healthy controls. Resting extracellular skin levels of histamine and histamine release to mast cell secretagogues, as measured by the microdialysis technique, were increased in involved psoriasis skin compared to normal skin in the controls. Plasma histamine, but not basophil histamine release, was significantly increased in the patients. Mast cells and lymphocytes were significantly increased in numbers in involved versus non-involved skin in the patients, the lymphocytes being predominantly T-lymphocytes expressing HLA-DR activation. During 6 months of ranitidine treatment, mean PASI score of 15.4 decreased to 5.8. The lymphocyte infiltration, but not mast cell numbers, was significantly reduced during treatment, and histamine release to mast cell secretagogues was normalized. These observations suggest that skin mast cells in active psoriasis are functionally hyperreactive. The biochemical findings together with the clinical effect of ranitidine indicate that histamine may be involved in the pathophysiology of psoriasis.
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In vitro anaphylactic reaction causes mast cell damage and histamine release from rat tissue. Histamine release is correlated with mast cell damage and both phenomena are simultaneously inhibited by various metabolic inhibitors, antipyretics, calcium lack and previous heating of the tissue at 45 degrees . The mast cell damage produced by antigen in sensitized rat tissues is morphologically similar to that caused by compound 48/80, both agents causing extrusion of granules. Mast cell damage and histamine release induced by antigen or by compound 48/80 are inhibited alike by several substances and conditions. It is suggested that in rats the histamine-releasing mechanism of the antigen-antibody reaction in anaphylaxis is very similar to that of compound 48/80.
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IT HAS BEEN SHOWN THAT, DEPENDING UPON THEIR CONCENTRATION, ANTIHISTAMINES ACT IN THREE DIFFERENT WAYS: (a) by competitive inhibition of histamine as already known; (b) by destroying mast cells and releasing histamine; and (c) by preventing mast cell damage and histamine release in anaphylaxis. Furthermore, antihistamines potentiated mast cell damage and histamine release by compound 48/80, when acting on guinea-pig tissues, and inhibited these same phenomena when acting on rat tissues. It is concluded that the effect of antihistamines in anaphylaxis is possibly due both to their competitive inhibition of histamine on smooth muscle receptors and to their inhibition of mast cell damage and histamine release by antigen.
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Abstract Thirty‐five synovial fluid (SF) specimens were examined for the presence of mast cells and for their histamine content. Mast cells were seen in SF cells from 27 of 35 fluids, and histamine was measurable in 19 of 34. There was a strong correlation between mast cell number and histamine content. No consistent relationship was found between either the mast cell number or histamine level and the patients' diagnoses, except that the 2 patients with systemic mastocytosis had markedly elevated values for both SF mast cell number and histamine content. SF mast cells from one of the mastocytosis patients were studied for histamine release; significant amounts of histamine were released upon exposure to anti‐human IgE, but not compound 48/80. Thus, mast cells similar to those present in connective tissue are frequently present in SF in numbers which correlate with SF histamine levels. These mast cells contain active proteases and are capable of degranulation. Mast cells were consistently present in large numbers in the SF of patients with systemic mastocytosis, but their numbers were highly variable in fluids of patients with other diseases.
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Histamine H4 receptor
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Bradykinin, as well as histamine which has been considered as one of the chemical mediators in immediate type allergic reaction, increases cyclic adenosine 3′ 5′-monophosphate (cAMP) of murine lymphocytes, especially T lymphocytes and it is also shown that both bradykinin and histamine suppress T cell mitogens (PHA-P, Con A) - induced proliferation of murine splenic lymphocytes.These results suggest that bradykinin as well as histamine may have some suppressive effect on cellular immunologicarle sponses. From this aspect the present experiment was undertaken to study the effect of chemical mediators such as bradykinin, histamine, serotonin and acetylcholineo n the production of antigen-inducedm igrationi nhibitoryf actors in the immune guinea pig peritoneal exudate cells. The results obtained were as follows(1) The antigen-inducedM IF production was remarkablys uppressed by the addition of bradykinin or histamine. The migration inhibition percent by the treatment of bradykinin (10-6-10-7M) or histamine (10-4-10-6M) was about the same and the dose response fashion was observed between the dose of the drug (bradykinin or histamine) added and the inhibition percent.(2) No suppressivee ffect on MIF productionw as observed by the treatment of serotonin or acetylcholine.(3) The suppressive effect of bradykinin or histamine on MIF production was observed when bradykinin or histamine was added immediately after the addition of antigen, but the suppressive effect slightly decreased when it was added 30-60 min after the addition of antigen. The suppressive effect decreased ren-arkably when it was added 2 hr after the addition of antigen.These findings suggest that bradykinin or histamine exerts its effects at an early stage in the MIF response, perhaps interfering with an antigendependents tage.(4) The suppressive effect of bradykinin or histamine on MIF production was only slightly blocked by the treatment of H1antagonist, but clearly blocked by the treatment of H2-antagonist or H2agonist.(5) No synergistic effect- of bradykinin and histamine was observed on the suppressive action of MIF production.
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The effect of immobilization, gentle handling and decapitation on the level of plasma histamine in Wistar rats was investigated. Mast cell deficient (Ws/Ws) rats were used to characterize the source of elevated histamine in plasma by stress, and the effect of nedocromil, a mast cell stabilizer, on histamine release was assessed in these models in vivo. The plasma histamine concentration of freely moving rats was 93.0±2.3 pmol/ml. Gentle handling produced a transient increase in plasma histamine level by 1.9-fold, whereas immobilization resulted in a longer-lasting elevation by 2.6-fold compared to that in the freely moving rats. Decapitation increased the plasma histamine level by 10- to 16-fold compared with that in the freely moving rats. No increase in plasma histamine was found in Ws/Ws rats exposed to stress. Nedocromil inhibited the increase in plasma histamine level induced by stress in a dose-dependent manner. These findings suggest that stress induces histamine release from mast cells in Wistar rats and the extent of this histamine release increases with the severity of stress. Nedocromil proved to be a good pharmacological tool to inhibit stress-induced release of mediators from mast cells.
Nedocromil
Compound 48/80
Nedocromil Sodium
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Histamine is a key chemical mediator in allergic inflammatory responses.The allergic inflammatory responses resulting from the release of histamine have been thought to be mediated only by the histamine H1 receptor.However,the discovery of a fourth histamine receptor and its expression on numerous immune organ and cells has induced a re-evaluation of the actions of histamine.The histamine H4R is involved widely in allergic inflammation and shown a important function in those immune responses. Histamine H4R selective antagonists have extremly high affinity to H4R and also demonstrate efficacy as anfi-inflammtory agents and immune modulator.The H4R antagonists appear to be a novel and potential therapy for a variety of allergic diseases.
Histamine H4 receptor
Allergic Inflammation
Mediator
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