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PubMed1986

Effects of histamine-receptor antagonists on histamine-stimulated renin secretion.

The effects of histamine H1- and H2-receptor antagonists on histamine-stimulated renin secretion were examined in anesthetized dogs. Tripelennamine (H1 blocker) further enhanced renin secretion in the presence of exogenous histamine. Moreover, tripelennamine alone increased renin secretion. These effects are probably due to non-specific properties of the drug and not to interaction of tripelennamine with H1 receptors. Conversely, cimetidine (H2 blocker) significantly inhibited histamine-induced increases in renin secretion, renal blood flow, and sodium excretion without any changes in mean arterial blood pressure or glomerular filtration rate. Cimetidine alone had no effect. We conclude that H2 receptors mediate the effect of histamine on renin secretion in dogs with innervated, intact kidneys.

Animals↗
PubMed1991

Effects of thioperamide, a histamine H3 receptor antagonist, on locomotor activity and brain histamine content in mast cell-deficient W/Wv mice.

The purpose of this study was to examine the effects of thioperamide, a histamine H3 antagonist, on the locomotor activity and the brain histamine content in mast-cell-deficient W/Wv mice. Thioperamide (12.5 and 25 mg/kg) showed significant increase in the locomotor activity of W/Wv mice, measured by a photo-beam system, 1 hr after the intraperitoneal injection. However, more than 75 mg/kg of thioperamide showed not only the reduction of the locomotor activity but also the inhibition of motor coordination measured by the rotarod performance. The increase in the locomotor activity by thioperamide was blocked by i. p. pretreatment with (R)-alpha-methyl-histamine, an H3 agonist, or pyrilamine, an H1 antagonist, or zolantidine, an H2 antagonist. The brain histamine content was decreased by thioperamide (12.5-75.0 mg/kg), 1 hr after administration. Thus, the blockade of histamine H3 receptor by thioperamide showed the activation of locomotor activity of mice, which may be mediated by H1 and/or H2 receptors. The present data support the hypothesis that central histaminergic neurons may be involved in the control of state of wakefulness.

Animals↗
PubMed1977

Purification of histamine receptor. (IV) Specificity of binding of various drugs to the histamine receptor-rich fraction and to solubilized binding sites.

Studies were made on tritiated histamine binding to the receptor-rich membrane fraction and solubilized sites and its displacement by various drugs. H1-Agonists and antagonists displaced histamine most effectively. A H2-agonist and atropine were less effective and propranolol, phentolamine and imidazole acetic acid had little effect. The solubilized binding sites showed the same specificity of binding as the membrane fraction. Membrane fragments had two binding constants, whereas solubilized sites had only one. Solubilized sites bound similar amounts of histamine and dibenamine: the latter was applied to intact tissue under conditions which would presumably cause specific binding to histamine receptors. These binding characteristics show that the method used was adequate for purification of histamine receptors from smooth muscle of cat small intestine.

Animals↗
PubMed1987

Effects of histamine on the metabolism of isolated rat hepatocytes: roles of H1- and H2-histamine receptors.

In isolated rat hepatocytes histamine stimulates in a dose-dependent fashion three of the major metabolic pathways: glycogenolysis (70-80% increase over basal), gluconeogenesis from lactate (50-60%), and ureagenesis (50-60%). It was observed that both H1 and H2 receptors mediate the action of histamine and that, in control hepatocytes, the H1-mediated action predominates over the H2. The H1-mediated effect diminished in the absence of extracellular calcium, whereas the H2-mediated action did not. Interestingly, in hepatocytes from hypothyroid rats, the H2 action increased and the H1-mediated effect decreased as compared to those in the controls, with an inversion in efficacy (i.e., H1 greater than H2 in the controls and H2 greater than H1 in cells from hypothyroid rats). Furthermore, it was observed that pertussis toxin treatment and forskolin both enhance the H2-mediated effects without altering the H1-mediated actions of histamine (i.e., H1 approximately equal to H2). The active phorbol ester, phorbol 12-myristate 13-acetate, did not alter the effect of the autacoid. In summary, the data show that histamine modulates liver metabolism through H1 and H2 receptors. The relative importance of the two receptor types in mediating the actions of histamine varies depending on the specific conditions used.

Animals↗
PubMed1992

Determination of histamine and polyamines in calcified tissues of mice: contribution of mast cells and histidine decarboxylase to the amount of histamine in the bone.

A simple method for determining histamine and polyamines in various tissues was devised. The method, however, could not be applied to calcified tissues, because the high concentration of Ca2+ in the extract interferes with the chromatographic separation of these amines. By treating the extracts from calcified tissues with K2CO3, we succeeded in removing the Ca2+, and the method could then be applied to determine the amines in bone tissues of mice. By using this method, we examined the contribution of mast cells and histidine decarboxylase (HDC) to the amount of histamine in the bone. The results indicate that (1) the HDC activity in the bone is the highest among the tissues of normal mice, and the histamine produced by the HDC in the bone is metabolized rapidly; (2) a major part of HDC in the bone is present in the bone marrow cells other than mast cells, and most of histamine in the bone is attributable to the histamine pooled in mast cells; (3) mast cells in the diaphysis are located largely along the endosteal lining; and (4) the method devised in this study may be useful for studying the roles of histamine (or mast cells) and polyamines in calcified tissues.

Animals↗
PubMed1977

Histamine metabolism in cluster headache and migraine. Catabolism of 14C histamine.

Various parameters of histamine metabolism were studied in patients with migraine, cluster headache and chronic paroxysmal hemicrania. These included urinary excretion of radioactivity and of 14C histamine and its metabolites, exhaled 14CO2 and fecal radioactivity after oral as well as subcutaneous administration of radioactive histamine. No marked deviation from the normal was found except in one patient with the cluster headache variant, chronic paroxysmal hemicrania, in whom an aberration in 14C histamine degradation seemed to be present. Only minute quantities of the 14C histamine metabolite C14 imidazoleacetic acid riboside seemed to be formed during a period with severe paroxysms. During a symptom-free period no deviation from normal was observed. The most likely explanation for this finding seems to be a defect in the conversion of imidazoleacetic acid to its riboside. This defect may possibly explain the increased urinary excretion of histamine in this particular patient. The relationship of this metabolic aberration to the production of headache still remains dubious for various reasons.

Biotransformation↗
PubMed1976

Histamine and peptic ulcer: a prospective study of mucosal histamine concentration in duodenal ulcer patients and in control subjects suffering from various gastrointestinal diseases.

In a prospective study the histamine content of the mucosa of the body of the stomach was measured in 100 patients consisting of control subjects, patients with duodenal ulcer and patients suffering from various gastrointestinal diseases. The histamine content was found to be 43 mug/g in male control subjects (median) while in duodenal ulcer patients levels attained were significantly lower by about 30 per cent. In all the other groups of patients histamine concentrations in gastric mucosa were found to be "normal". Since in most species it is extremely diffcult to alter the mucosal histamine concentration by any form of treatment, the diminished histamine content of the gastric mucosa in patients with duodenal ulcer seems remarkable. Among several possible explanations offered for this finding we think the most likely is that histamine release is increased in duodenal ulcer disease.

Duodenal Ulcer↗
PubMed1980

[Effects of acetylcholine- and histamine inhalations also of hypoxia on the arterial plasma-histamine concentration (experiments on dogs). III. Communication (author's transl)].

Inhalation of acetylcholine causes increased histamine concentration in the arterial plasma. This increase is smaller than that following allergen inhalation. The increase in Edyn following ACH inhalation may be related to the histamine released to only a very limited extent. Comparison of the effects of histamine inhalation and allergen inhalation on Edyn and plasma histamine concentration leads to the assumption that sensory receptors are located nearer to the surface of the mucosa than that of the mast cells. Hypoxemia is followed by a slight increase in the arterial plasma histamine concentration. The increase in Edyn corresponds to that caused by allergen inhalation although the increase in Edyn and that in the plasma histamine are much smaller.

Acetylcholine↗
PubMed1988

Histamine and Nt-methylhistamine in the circulation during intravenous infusion of histamine in normal volunteers.

Plasma levels of histamine and Nt-methylhistamine were measured simultaneously by high performance liquid chromatography during the intravenous infusion of histamine acid phosphate in six normal volunteers. Progressive, dose-related increases in plasma histamine were noted, reaching a maximum value of 3.1 +/- 0.14 ng ml-1 corresponding to a maximum infusion rate of 180 ng kg-1 min-1 (means +/- SEM). Increases in plasma histamine were accompanied by a significant dose-related fall in mean diastolic blood pressure (baseline 74.0 +/- 4.4 mm Hg falling to 60.0 +/- 3.3 mm Hg at maximum infusion rate, p less than 0.001) and an increase in pulse rate (baseline 76.3 +/- 2.8 beats min-1 rising to 89.24 beats min-1 at maximum infusion rate, p less than 0.05). All subjects exhibited facial flushing, the threshold plasma histamine level for this effect being 1.3 +/- 0.15 ng ml-1 corresponding to an infusion rate of 60 ng kg-1 min-1. Elevation of plasma Nt-methylhistamine was seen in only one subject, who exhibited a level of 0.5 ng ml-1 at the highest infusion rate. These results suggest that measurements of plasma Nt-methylhistamine are unlikely to provide a useful index of histamine release into the circulation.

Adult↗
PubMed1975

Effect of histamine H2-receptor and beta-receptor blockade on histamine-, orciprenaline- and prostaglandin-stimulated frequency of the isolated guinea-pig atrium.

For the oxyntic cell of the stomach the hypothesis was forwarded by Grossmann and Konturek [1] that, if one of its three receptors is blocked, the physico-chemical properties of the two others are changed in such a way that they respond less sensitively to their specific stimulation. This hypothesis was tested for the heart by studying the effect of histamine-H2-receptor- and beta-receptor-blockade on the orciprenaline-, histamine-, and prostaglandin E1-stimulated frequency of the spontaneously beating isolated guinea-pig atrium. Therefore cumulative dose response curves were established for orciprenaline, histamine and prostaglandin E1 (PGE1) alone or in the presence of metiamide or pindolol. (1) The beta-blocker pindolol inhibited the effect of orciprenaline in a competitive manner, without having an effect on histamine- and PGE1-stimulation. (2) The histamine H2-receptor blocker metiamide inhibited the histamine response competitively. (3) In contrast to pindolol, metiamide inhibited the PGE1-stimulated rise in atrial frequency, most obviously non- or uncompetitively. From these results it is evident that in the heart the particular inhibitors, at least at the receptor site, act rather specifically without affecting neighbouring receptors and that metiamide influences the PGE1-response in a way different from the receptor site.

Animals↗
PubMed1984

An attempt to produce an antibody of histamine and histamine derivatives.

Three conjugates of different histamine derivatives to bovine serum albumin were prepared, and an attempt was made to determine whether antibody against histamine and histamine derivatives could be produced in rabbits by immunization with these conjugates. Antibody produced by immunization with bovine serum albumin-succinylhistamine conjugate could not recognize the hapten moiety of the immunogen. Immunization of rabbits with conjugate of bovine serum albumin and p-[2-(N alpha-trifluoroacetylhistamine)azo]benzoic acid resulted in the production of antibody to N alpha-trifluoroacetylhistamine. The antibody had a specificity for histamine metabolites and their derivatives. However, the antibody also showed a small but not negligible affinity for trifluoroacetylated serotonin, norepinephrine and aniline, indicating that the antibody specificity was directed mainly to the trifluoroacetamide group. After immunization of rabbits with bovine serum albumin and p-[2-(N alpha-propionylhistamine)azo]benzoic acid conjugate, antibody against N alpha-propionylhistamine could be produced. However, the antibody had a very low affinity even for N alpha-propionylhistamine. Specific antibody to histamine and histamine derivatives could thus not be produced by immunization with the present hapten-carrier conjugates.

Animals↗
PubMed1979

An experimental study on histamine H2-receptor antagonist on calcium, gastrin and histamine induced gastric acid secretion in rat.

The suppressive effect of histamine H2-receptor antagonist, cimetidine, on gastric secretion was investigated in Ghosh-Schild rat. The study above was done in basal state under infusing normal saline (1 ml/h) and stimulated state by histamine-di-chloride (3.5 mg/kg-h), tetragastrin (50 mcg/kg-h) or calcium chloride (4 mg/kg-h). Dose related increase of cimetidine (1.7, 3.5, 7.0 and 14.0 mg/kg-h) were observed and correlated with the degree of inhibition of acid secretion. Cimetidine had a potent inhibitory activity on either basal and stimulated acid output by the agents above. Basal acid secretion was completely abolished by 3.5 mg/kg-h of cimetidine to the level of anacidity. The degree of inhibition by the same dose of cimetidine was different among the agents used as stimulant on acid secretion and it followed in the order of calcium, gastrin and histamine subsequently. This study indicated that histamine H2-receptor participated the gastric secretion induced by either gastrin or calcium other than histamine itself. This fact indicated the important role of endogenous histamine in gastric secretion induced by calcium and gastrin.

Animals↗
PubMed1989

Formation of chloramine derivatives of histamine: role of histamine chloramines in bronchoconstriction.

Hypochlorous acid generated by myeloperoxidase reacts with histamine to produce chloramines. At pH 7, one mole of histamine monochloramine (HisCl) was generated per mole of H2O2 provided as substrate for myeloperoxidase. At pH 5, one mole of histamine dichloramine (HisCl2) was generated per two moles of H2O2. HisCl and HisCl2 had two and four oxidizing equivalents per molecule, respectively. In vitro, 30 microM HisCl and HisCl2 induced mepyramine-sensitive guinea pig lung parenchyma contraction with 89 and 56 percent of the response of an equivalent concentration of histamine. Pretreatment of lung strips with chloramines reduced the subsequent contractile response of the tissues to methacholine. These results suggest that H-1 histamine receptors provide for targeting of histamine chloramines to pulmonary tissue which may facilitate modification of tissue responses.

Animals↗
PubMed1982

Tissue distribution of histamine in a mutant mouse deficient in mast cells: clear evidence for the presence of non-mast-cell histamine.

The contents of histamine in various tissues of mutant mice deficient in mast cells (W/Wv) and in congenic normal mice (+/+) were determined by high-performance liquid chromatography and were compared. In spite of the absence of mast cells in W/Wv mice, the histamine content of their whole bodies was about 5-10% of that of +/+ mice. The skin, heart and lungs of W/Wv mice contained negligible amounts of histamine (about 2% of that in +/+ mice), but the liver, kidneys and spleen contained appreciable histamine (8-15% of that in +/+ mice), and the brain and stomach contained much histamine (45 and 34%, respectively, of that in +/+ mice). These results indicate the presence of non-mast-cell histamine, especially in the brain and stomach, where it may play important physiological roles.

Animals↗
PubMed2005

Histamine dehydrogenase from Rhizobium sp.: gene cloning, expression in Escherichia coli, characterization and application to histamine determination.

The gene encoding histamine dehydrogenase in Rhizobium sp. 4--9 has been cloned and overexpressed in Escherichia coli. The coding region of the gene was 2,079 bp and encoded a protein of 693 amino acids with a calculated molecular mass of 76,732 Da. This histamine dehydrogenase was related to histamine dehydrogenase from Nocardioides simplex (54.5% identical), trimethylamine dehydrogenase from Methylophilus methylotrophus (39.3% identical) and dimethylamine dehydrogenase from Hyphomicrobium X (38.1% identical), which have a covalent 6-S-cysteinyl flavin mononucleotide and a [4Fe--4S] cluster as redox cofactors. Sequence alignment and a UV-visible absorption spectrum supported the presence of these cofactors in this histamine dehydrogenase. The investigation of the enzymatic properties suggested that this enzyme exhibited the most excellent substrate specificity toward histamine among all amine oxidases or dehydrogenases found to date. The recombinant enzyme was able to be used for the colorimetric determination of histamine, which gave a linear calibration curve and identical data with conventional methods.

Animals↗
PubMed1999

Pharmacologic regulation of histamine release by the human recombinant histamine-releasing factor.

BACKGROUND: The recently cloned human recombinant IgE-dependent histamine releasing factor (HrHRF) was initially thought to stimulate histamine release from human basophils from a subpopulation of allergic donors by interacting with the IgE molecules on the surface of these cells. Additional data suggest that HrHRF exerts its biologic effects by binding to a distinct cell surface structure and not to IgE. OBJECTIVE: To address the hypothesis that the HrHRF signaling pathway is distinct from the classical high-affinity IgE receptor (FcepsilonRI) pathway, we used pharmacologic agents known to affect basophil histamine release. METHODS: In this report we compared the effect of staurosporine, Bis II, Gö 6976, rottlerin, and pertussis toxin on histamine release from human basophils mediated by the following stimuli: HrHRF, polyclonal human anti-IgE antibody, and antigen, as well as the IgE-independent stimulus, FMLP. RESULTS: None of these modulators, except rottlerin, could differentiate histamine release induced by anti-IgE or antigen from that induced by HrHRF. Rottlerin enhanced HrHRF-mediated histamine release and dose dependently blocked FMLP-mediated release without affecting basophil activation by either anti-IgE or antigen. CONCLUSION: These data suggest a unique signaling pathway for HrHRF and thus strengthen the hypothesis that HrHRF binds to a specific receptor other than IgE.

Acetophenones↗
PubMed2001

Src homology 2 domain-containing inositol 5' phosphatase is negatively associated with histamine release to human recombinant histamine-releasing factor in human basophils.

BACKGROUND: The human recombinant histamine-releasing factor (HrHRF) acts as a complete stimulus for histamine release and IL-4 secretion from a subpopulation of highly allergic donor basophils, termed IgE(+) basophils. Additionally, IgE(+) basophils release histamine to other secretogues, IL-3, and deuterium oxide. We hypothesized that IgE(+) basophils were hyperreleasable. OBJECTIVE: Deficiencies in early signal transduction events associated with Fc(epsilon)RI lead to a nonreleasable phenotype, whereas the Src homology 2 domain--containing inositol 5' phosphatase (SHIP) knockout mice have hyperreleasable mast cells. The purpose of this study was to ascertain whether a difference in intracellular signaling molecules could explain the hyperreleasable phenotype of human IgE(+) basophils. METHODS: Basophils were purified by means of double Percoll gradients and negative selection with magnetic beads. Cell lysates were Western blotted for the tyrosine kinases Lyn and Syk and the phosphatase SHIP. Additionally, histamine release to HrHRF was performed in addition to real-time RT-PCR to investigate mRNA for SHIP. RESULTS: We show a striking negative correlation between the amount of SHIP protein per cell equivalent, but not Lyn or Syk, and maximum histamine release to HrHRF. This deficiency of SHIP was observed in basophils, but not lymphocytes or monocytes, of these IgE(+) donors. Additionally, levels of mRNA for SHIP did not differ between IgE(+) and IgE(-) donor basophils, which is consistent with a posttranscriptional mechanism of protein regulation. SHIP and phosphatidylinositol 3-kinase reciprocally regulate phosphatidylinositol (3,4,5) triphosphate levels. We also demonstrated that Ly294002, the phosphatidylinositol 3 kinase inhibitor, prevented HrHRF-induced histamine release in IgE(+) donor basophils. CONCLUSION: Taken together, these data suggest that the hyperreleasability of IgE(+) donors is associated with low levels of SHIP and implicate SHIP as an additional regulator of secretion in human basophils.

Basophils↗
PubMed1995

Effects of PBMC-derived histamine-releasing factors on histamine release from human skin and lung mast cells.

BACKGROUND: A field of study which has attracted much recent interest is the ability of mononuclear cells and neutrophils to interact with histamine releasing cells by production of specific histamine releasing factors (HRFs). However, almost all of these studies have been performed on basophils rather than human mast cells. OBJECTIVE: We have investigated the effects of lyophilized fractions of HRF preparations on histamine release from human skin and lung mast cells. METHODS: Lyophilized fractions of HRF preparations include crude supernatant from mononuclear cell/platelet (crude), void peak from anion exchange chromatography column (void), second peak from anion exchange chromatography (peak 2), neutrophil-activating peptide-2 (NAP-2), which was purified from void peak at molecular weight of 8-12 kDa, and monocyte chemotactic-activating factor (MCAF). Mast cells were enzymatically dispersed. RESULTS: Crude (24.2 micrograms/mL-2.42 mg/mL), void (5.4 micrograms/mL-0.54 mg/mL), peak 2 (3.5 micrograms/mL-0.35 mg/mL), and NAP-2 (1-20 micrograms/mL) failed to release histamine from lung mast cells. In skin mast cells, only higher concentrations of crude and void caused minimal release of histamine. MCAF up to micromolar concentrations failed to have an effect on mast cells from either source. However, these HRFs induced histamine release from human basophils. We also explored whether HRFs and stem cell factor could act as either priming agents for each other or for anti-IgE. The response of skin mast cells to all these preparations was not enhanced by preincubation in stem cell factor at 1 ng/mL, nor did the HRFs and MCAF enhance the response of skin mast cells to anti-IgE. CONCLUSION: These results suggest that these HRFs have no significant effect on dispersed human cutaneous and lung mast cells.

Basophils↗