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PubMed1982

Inhibition by calcium antagonists of histamine release and calcium influx of rat mast cells: difference between induction of histamine release by concanavalin A and compound 48/80.

The relation between calcium influx and histamine release from rat mast cells was investigated. When purified mast cells pretreated with a calcium antagonist (MnCl2 or methoxyverapamil (D-600)) were exposed to concanavalin A or compound 48/80 in Tyrode solution (pH 7.4) at 37 degrees C, the calcium antagonists inhibited the extracellular calcium-dependent component of concanavalin A-induced histamine release. MnCl2 also inhibited the extracellular calcium-dependent component of compound 48/80-induced histamine release, whereas D-600 did not inhibit the release. D-600 inhibited the 45Ca uptake induced by concanavalin A, but did not inhibit the 45Ca uptake induced by compound 48/80. It was found that the inhibitory action of calcium antagonists depended on the uptake of extracellular calcium. These observations suggest that concanavalin A and compound 48/80 stimulate different mechanisms of calcium influx. Studies on inactivation of the mechanisms of calcium influx showed that calcium influx into cells activated by concanavalin A stopped when concanavalin A was washed out, whereas the influx activated by compound 48/80 was still operative after compound 48/80 had been washed out.

Animals↗
PubMed1984

Histamine-releasing activity (HRA). III. HRA induces human basophil histamine release by provoking noncytotoxic granule exocytosis.

Histamine-releasing activity (HRA) is an approximately 10,000-15,000 dalton, protease-sensitive factor that induces the rapid liberation of histamine from human basophils. Production of HRA by human peripheral blood mononuclear cells in vitro is augmented by concanavalin A or antigen, suggesting a mechanism whereby lymphocytes may regulate basophil mediator release in vivo. In order to determine whether HRA provokes conventional exocytosis of basophil granules or, alternatively, results in mediator release by some other mechanism such as vesicular transport or cytotoxicity, we investigated the ultrastructural features of human blood basophils purified over Percoll and exposed to HRA in vitro. HRA preparations induced a noncytotoxic pattern of basophil degranulation very similar to that previously observed in basophils triggered to release histamine in response to specific antigen, C5a, or mannitol. Thus, cytoplasmic granules were extruded singly through multiple separate points of fusion between perigranular membranes and the plasma membrane. Degranulating basophils exhibited plasma membrane activation but lacked a polarized configuration. By contrast, those basophils exposed to HRA that did not exhibit evidence of degranulation displayed a single elongated cellular process. The development of this polarized cellular configuration, similar in some respects to that of uropod-bearing motile guinea pig basophils, may have reflected chemokinetic or chemotactic effects of preparations containing HRA activity.

Antigens↗
PubMed1996

Comparative ultrastructural morphology of human basophils stimulated to release histamine by anti-IgE, recombinant IgE-dependent histamine-releasing factor, or monocyte chemotactic protein-1.

An ultrastructural analysis of human basophils stimulated with anti-IgE, recombinant histamine-releasing factor (rHRF), or monocyte chemotactic protein-1 (MCP-1) (compared with unstimulated cells) was performed. Partially purified peripheral blood basophils were prepared for electron microscopy at time points known to precede histamine release and at half-maximum histamine release times for each secretagogue. Activation morphologies associated with stimulation included granule-vesicle attachments, piecemeal degranulation, anaphylactic degranulation, and uropod formation. These features were qualitatively similar in the stimulated samples. Quantitative differences were evident, however, when stimulated samples were compared with controls or at different time points after stimulation with a single agent or when individual secretagogues were compared. All stimulated samples differed quantitatively from the control samples. Rank orders for morphologic activation events revealed that the most effective trigger for anaphylactic degranulation was anti-IgE > MCP-1 > rHRF, whereas the most effective trigger for uropod formation was rHRF > anti-IgE > MCP-1. Rank orders for piecemeal degranulation and granule-vesicle attachments were the same: MCP-1 > anti-IgE > rHRF. Important relationships among these anatomic events reveal that the development of motile configurations is not associated with the development of secretion morphologies and that piecemeal degranulation precedes and is inversely related to anaphylactic degranulation in stimulated samples.

Antibodies, Anti-Idiotypic↗
PubMed1998

Histamine and cutaneous nociception: histamine-induced responses in patients with atopic eczema, psoriasis and urticaria.

Having observed altered itch and flare reactions after histamine application in patients with atopic eczema, we tried to determine these reactions in patients with urticaria and psoriasis. We investigated 16 healthy non-atopic subjects, 16 atopics in an eczema-free interval, 16 with acute atopic eczema, 16 with urticaria and 16 with psoriasis. Histamine was iontophoretically applied. The resulting sensations were rated on a visual analogue scale. Flare areas were measured 6 min after stimulation. Itch ratings of urticaria and psoriasis patients did not differ significantly from controls, whereas both atopic groups, regardless of acute or symptom-free state, reported significantly reduced intensity of itching. Flares were significantly diminished in all subjects with acute skin disease (psoriasis, urticaria and atopic eczema), regardless of diagnosis. However, flares were "normal" in symptom-free atopics and were not significantly different from controls. In conclusion, all "acute" patients showed a diminished axon-reflex function, possibly due to a downregulation of C-fiber responsiveness to histamine or an increased turnover rate of inflammatory mediators. Both atopic groups reported weaker itching, suggesting altered central nervous processing of itch.

Acute Disease↗
PubMed1984

Astemizole, a potent histamine H1-receptor antagonist: effect in allergic rhinoconjunctivitis, on antigen and histamine induced skin weal responses and relationship to serum levels.

The efficacy of astemizole, a new, long acting, oral histamine H1-receptor antagonist was compared to placebo for the treatment of allergic rhinitis and conjunctivitis during the grass pollen season of 1982. Sixty-three patients with a positive skin prick test to grass pollen and current symptoms participated in an 8 week, double-blind, randomized study. Astemizole, 10 mg, was significantly better than placebo in alleviating both nose (P less than 0.05) and eye (P less than 0.01) symptoms despite significantly greater use of the reserve medication, clemastine, by the placebo group (P less than 0.003). There was a lag period of 5 days after initiation of therapy before treatment benefit became manifest. Subdivision of nasal symptoms indicated significant improvement compared to placebo over the 8 weeks for sneezing (P less than 0.05) and runny nose (P less than 0.05) but not blocked nose. The absence of effect on nasal blockage was confirmed by parallel measurement of nasal calibre by body plethysmography. The antihistaminic potency of astemizole was indicated by an 80% inhibition of the histamine induced skin weal response after 8 weeks therapy. A positive correlation was found between serum drug levels and % inhibition of histamine skin weal (r = 0.64, P less than 0.001). Astemizole was free from adverse sedative or anticholinergic effects but did cause a mean increase in weight of 1.3 kg (P less than 0.01) after 8 weeks therapy, not found with placebo.

Adolescent↗
PubMed1989

Comparison of histamine assay methods in measuring in vitro-induced histamine release in patients with allergic rhinitis.

histamine release tests using whole blood were applied in testing in vitro Type I birch allergic reaction in two patients with allergic rhinitis. Heparinized blood was incubated with varying dilutions of allergen for 30 min at +37 degrees C. After centrifugation of the blood, plasma was separated and the liberated histamine was analysed by histamine radio enzyme assay (REA), high performance liquid chromatography (HPLC) with post-column derivatization system or radio immuno assay (RIA), and the results obtained by these methods were compared. REA and HPLC gave similar results, while RIA gave somewhat higher values, but was less sensitive.

Adolescent↗
PubMed1993

Comparison of fiberglass-based histamine assay with a conventional automated fluorometric histamine assay, case history, skin prick test, and specific serum IgE in patients with milk and egg allergic reactions.

A microfiberglass-based histamine assay (HRM) was compared with an automated fluorometric histamine assay (HRA). Twenty-four subjects with and 24 without a case history (CH) of milk and/or egg allergy were tested by HRM and HRA, skin prick test (SPT), and specific serum IgE (RAST). Six different concentrations of milk, egg, and anti-IgE were used to stimulate washed leukocytes (250 microliters for HRA) and whole blood samples (25 microliters for HRM) in parallel. When we compared scores representing basophil sensitivity, correlation coefficients (rs) were positive (r(anti-IgE) = 0.88, r(egg) = 0.95, r(milk) = 0.88, P < 0.001), but no significant correlations were found after exclusion of the negatives in both tests. In some individual dose-response curves, the scores obtained by HRM were shifted to higher allergen and anti-IgE concentrations. A high degree of concordance was found in positive and negative responses between the two tests: anti-IgE 91%, egg 92%, milk 86%. Finally, we found a good concordance between, on one side, HRM and, on the other, CH, SPT, and RAST (HRM vs. CH/SPT/RAST): egg 92/82/82%; milk 89/74/67%. We conclude that HRM is in good qualitative, but poor quantitative, agreement with the autoanalyzer-based fluorometric histamine assay.

Adolescent↗
PubMed1984

Role of histamine in the aetiology of byssinosis. II. Lung histamine concentrations in guinea pigs chronically exposed to cotton and flax dusts.

Data presented in this study support the finding that cotton and flax dusts contain agents which potentiate the formation or accumulation of histamine or both in the lungs of guinea pigs exposed to dust, and that such agents are present at much higher levels in cotton dust than in flax dust. The potentiating effect may be through the recruitment of mast cells into the lung. Both cotton and flax dusts contain methylating enzyme inhibitory agents, whereas cotton dust also contains agents that inhibit histaminase activity; flax dust contains agents potentiating histamine activity. These agents working together result in the accumulation or depletion of histamine observed in the different groups of animals exposed to either cotton or flax dust in this study.

Animals↗
PubMed1993

Dynamics of the skin blood flow response to histamine. Comparison of the effects of cetirizine and loratadine on the skin response to a histamine dry prick test monitored with laser-Doppler flowmetry.

In previous studies, we noticed that intradermal injection of histamine solutions might significantly complicate the interpretation of clinical data and of laser-Doppler flowmetry recordings (LDF). Therefore, we used the histamine dry skin prick test (HPT) for pharmacological studies. In this study, LDF monitoring of the physiological skin response to histamine was made in a randomized, placebo-controlled, double-blind study comparing the in vivo anti-H1 activity of cetirizine (10 mg) or loratadine (10 mg), 6 h after a single oral intake. As compared with responses recorded after intake of placebo, LDF readings performed at HPT sites (increase in LDF signal) and at 1 cm from HPT (reduction of LDF signal) conclusively illustrate the stable and almost complete blockade of H1 receptors by cetirizine. In vivo effects obtained with loratadine were considered weaker because (1) there was no significant influence of loratadine on the blood flow recorded at HPT sites, (2) a significant reduction at 1 cm from HPT sites was observed only after a lag phase (> or = 10 min) and (3) there were significantly higher skin perfusion levels at 1 cm from HPT sites between 6 and 10 min after the test under loratadine as compared with cetirizine. Hence, multipoint probing with LDF over time appears as a sensitive method for discriminating response profiles between two anti-H1 agents. Furthermore, this is the first time that anti-H1-related changes of the dynamics of expansion of the flare response have been demonstrated.

Adult↗
PubMed1975

Hypothalamic 24-hour rhythms in histamine, histidine, decarboxylase and histamine-N-methyltransferase.

Twenty-four hour rhythms of histamine (H), its biosynthetic enzyme, L-histidine decarboxylase (EC 4.1.1.22, HD) and its inactivation enzyme, histamine N-methyltransferase (EC 2.1.1.8, HMT) were assayed in the 63-day-old male rat hypothalamus using a modified single isotopeenzyme microassay. H was found to have a 24-h rhythm with a maximum concentration at 11:00 h (lights on 10:00-22:00 h) and a minimum at 23:00 h. In vitro HD and HMT activities were also found to have 24-h rhythms with peak activites in both occurring at 04:00 h. HMT also had a broad secondary peak throughout the day, whereas HD activity during the day was dominated by a mid-light trough at 16:00 h. These rhythms are considered significant for evaluation of the control and physiological role of histamine in the mammalian hypothalamus.

Animals↗
PubMedDate not supplied

Relationship of histamine-releasing factors and histamine-releasing inhibitory factors to chemokine group of cytokine.

The release of mediators from mast cells and basophils represents the central event in the development of immediate hypersensitivity reactions with release of substances such as histamine, Leukotrienes C4/D4, Platelet Activating Factor (PAF), and Prostaglandin D2. Cytokines such as IL-1, TNF alpha, and IL-4 may also be secreted. Histamine Releasing Factors (HRF) are cytokine-like molecules that interact with basophils and/or mast cells to cause cell activation and secretion of mediators. Histamine release is the best characterized of these and has been used as the assay for HRFs, but a wide variety of inflammatory mediators can potentially be secreted. We believe this type of cell to cell communication to be important in tissue inflammation, in which infiltrating cells may produce HRFs in proximity to infiltrating basophils and/or mast cells and cause them to degranulate. Such a reaction appears to be independent of IgE antibody, may no longer require the presence of any inciting antigen, and appears to be pertinent to the allergic late phase reaction as it occurs in the nose, lungs, and skin. It is thought that an ongoing antigenic stimulus, as seen in seasonal or perennial allergic rhinitis and asthma, or in certain types of urticaria, or in atopic dermatitis, leads to a perpetuating inflammatory reaction that persists for many weeks or months. A chronic inflammatory reaction of this sort appears to be required for an allergic reaction (IgE mediated) to manifest as an allergic disease. The relationship of HRF to the chemokine group of cytokine-like molecules and the importance of HRF in the pathogenesis of bronchial hyperreactivity and asthma has been reviewed in this paper.

Basophils↗
PubMed1985

Antramine (antral histamine) antagonizes somatostatin inhibition on endogenous gastrin-induced gastric secretion. A new hypothesis for the role of histamine in gastric secretion regulation.

The effects of antramine, an antral histamine (AH), and of synthetic histamine (SH) on acid, pepsin, and gastrin responses to meals alone or in combination with somatostatin were studied in dogs equipped with a Heidenhain pouch. Food-induced acid secretion was potentiated by AH and only slightly increased by SH. Pepsin secretion was increased by AH and decreased by SH. Both AH and SH suppressed the inhibitory activity of somatostatin on food-induced secretion. AH potentiated gastrin response to feeding but decreased it when somatostatin was added to the meal. Since acid secretion was unrelated to gastrin response, it would appear that the secretory effects of AH involve a direct action on secreting cells, itself based on the suppression of somatostatin inhibition. Gastric secretion is probably related to gastrin efficacy on secreting cells, which would result from the antagonistic effects of somatostatin and AH. These data suggest an alternative hypothesis concerning the role of histamine in the control of gastric secretion.

Amino Acids↗
PubMed1980

Influence of oxotremorine on histamine level and histamine synthesis in the rat brain.

The i.p. administration of oxotremorine (2 mg/kg) produced a decrease of both formation of 14C-histamine and the activity of specific histamine-synthetizing enzyme--histidine decarboxylase (HD). Oxotremorine had no effect on histamine level in the brain when given alone, but lowered the amine content in L-histidine-treated rats. All of these effects of oxotremorine were antagonized by atropine sulphate, but not by atropine methyl nitrate--a cholinolytic drug which does not penetrate the blood-brain barrier. Presented findings indicate a possibility of ACh--HI interaction in the rat brain. Possible mechanism of oxotremorine action is discussed.

Acetylcholine↗
PubMed1985

A role for histamine and histamine H2-receptors in non-opiate footshock-induced analgesia.

Scrambled DC current applied to the hind paws of rats caused an analgesic response that was inhibited by the histamine H2-receptor antagonists cimetidine, ranitidine and oxmetidine, but not by high doses of naloxone (the opiate antagonist), or other transmitter receptor antagonists. In contrast, AC current applied to all paws produced analgesia that was blocked by naloxone, but not cimetidine, showing the independence of these systems. These findings indicate a specific role for histamine and H2-receptors as mediators of endogenous non-opiate analgesia. In addition, a combination of cimetidine and naloxone did not abolish either form of footshock analgesia, implying the existence of a non-opiate, non-H2, endogenous pain-relieving system. These results also suggest that drugs capable of penetrating the brain and stimulating H2-receptors might have analgesic properties.

Animals↗
PubMed2006

A chemical switch for the modulation of the functional activity of higher homologues of histamine on the human histamine H3 receptor: effect of various substitutions at the primary amino function.

In an effort to establish the structural requirements for agonism, neutral antagonism, and inverse agonism at the human histamine H(3) receptor (H(3)R) we have prepared a series of higher homologues of histamine in which the terminal nitrogen of the side chain has been either mono- or disubstituted with several aliphatic, alicyclic, and aromatic moieties or incorporated in cyclic systems. The novel ligands have been pharmacologically investigated in vitro for their affinities on the human H(3)R and H(4)R subtypes by radioligand displacement experiments and for their intrinsic H(3)R activities via a CRE-mediated beta-galactosidase reporter gene assay. Subtle changes of the substitution pattern at the side chain nitrogen alter enormously the pharmacological activity of the ligands, resulting in a series of compounds with a wide spectrum of pharmacological activities. Among the several neutral H(3)R antagonists identified within this series, compounds 2b and 2h display an H(3)R affinity in the low nanomolar concentration range (pK(i) values of 8.1 and 8.4, respectively). A very potent and selective H(3)R agonist (1l, pEC(50) = 8.9, alpha = 0.94) and a very potent, though not highly selective, H(3)R inverse agonist (2k, pIC(50) = 8.9, alpha = -0.97) have been identified as well.

Amines↗
PubMed1993

Histamine analogues, XXXV: 2-substituted histamine derivatives containing classical moieties of H2-antagonists--a novel class of H1-agonists.

A new type of H1-agonists resulted from the combination of the essential histamine structure with parts of H2-antagonists. 2,4-Disubstituted imidazole derivatives were synthesized by reaction of imidic acid methyl esters with 1,3-dihydroxypropanone, 1,4-dihydroxybutanone or 2-oxo-4-phthalimido-1-butylacetate in liquid NH3. The imidazole intermediates were converted into histamine analogues by simple deprotection, Gabriel synthesis followed by deprotection, or by side-chain elongation via the nitriles and final hydrogenation. The new compounds were screened for H1-activity on the isolated guinea-pig ileum and for H2-antagonistic activity on the isolated guinea-pig right atrium. The substances are comparably weak H1-agonists and moderate H2-blockers.

Animals↗
PubMed1982

High-affinity binding of [3H]doxepin to histamine H1-receptors in rat brain: possible identification of a subclass of histamine H1-receptors.

The binding of the radioactively labeled tricyclic antidepressant, [3H]doxepin, to rat brain tissue was examined. Scatchard plots of specific [3H]doxepin binding indicated the presence of two distinct binding sites. The equilibrium dissociation constant (KD) of the high-affinity site was 0.020 nM with a maximal binding capacity (Bmax) of 13.7 fmol/mg protein. The corresponding values for the high-affinity site were 3.6 nM and 740 fmol/mg protein, respectively. The high-affinity site was sensitive to competition by pharmacologically relevant concentrations of histamine H1 antagonists such as pyrilamine (KD = 1.0 nM), diphenhydramine (KD = 20 nM), d-chlorpheniramine (KD = 1.7 nM), and 1-chlorpheniramine (KD = 97 nM). The Bmax for [3H]doxepin binding to the high-affinity H1-receptor, however, was approximately 10% of the Bmax obtained using [3H]pyrilamine to label the H1-receptor. Various tricyclic antidepressants were very potent inhibitors at the high-affinity [3H]doxepin site. Their potencies, however, did not correlate with their potencies previously reported for the H1-receptor. The regional distribution of [3H]doxepin high-affinity sites correlated with the known distribution of H1-receptors in the rat brain. These results suggest that [3H]doxepin is binding to a subclass of histamine H1-receptors.

Animals↗