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At least 541 records · Page 30Linked to original sources
PubMed1996

Inverse agonism of histamine H2 antagonist accounts for upregulation of spontaneously active histamine H2 receptors.

Histamine H2 receptors transfected in Chinese hamster ovary (CHO) cells are time- and dose-dependently upregulated upon exposure to the H2 antagonists cimetidine and ranitidine. This effect appears to be H2 receptor-mediated as no change in receptor density was observed after H1 or H3 antagonist treatment or after incubation with the structural analogue of cimetidine, VUF 8299, which has no H2 antagonistic effects. By using transfected CHO cells expressing different densities of wild-type H2 receptors or an uncoupled H2Leu124Ala receptor, the histamine H2 receptor was found to display considerable agonist-independent H2 receptor activity. Cimetidine and ranitidine, which both induce H2 receptor upregulation, actually functioned as inverse agonists in those cell lines displaying spontaneous agonist-independent H2 receptor activity. Burimamide, on the other hand, was shown to act as a neutral antagonist and did as expected not induce H2 receptor upregulation after long-term exposure. The displayed inverse agonism of H2 antagonists appears to be a mechanistic basis for the observed H2 antagonist-induced H2 receptor upregulation in transfected CHO cells. These observations shed new light on the pharmacological classification of the H2 antagonists and may offer a plausible explanation for the observed development of tolerance after prolonged clinical use.

Animals↗
PubMed1976

[Interference between histamine liberation and drugs used in anesthesiology. Prevention and treatment of the complications of histamine liberation].

The authors report the complications associated with the administration of some anaesthetics using propanidide. In one of the controls, premedication using an antihistamine was sufficient to avoid, during a third administration of propanidide, complications which included a fall in blood pressure and which had occurred when the second anaesthetic had been given. In one patient with high plasma histamine concentrations, circulatory arrest occurred during the second and third anaesthetic, despite meclastinum. Only the addition of a glucocorticoid to the premedication made possible an anaesthetic without problems. During a third propanidide anaesthetic given to this same patient, we were able to confirm our hypothesis by a premedication combining meclastinum and a glucocorticoid, despite the high plasma histamine level found. In certain other cases, however, plasma histimine concentration did not increase despite the development of erythema and urticaria of the face and neck. Serious complications were successfully dealt with using a combination of glucocorticoids, adrenaline derivatives and an antihistamine.

Anaphylaxis↗
PubMed1977

Effect of mepyramine, a histamine H1-, and burimamide, a histamine H2-receptor antagonist, on ovum implantation in the rat.

Systemic administration to rats of a combination of mepyramine, a histamine H1-, and burimamide, a histamine H2-receptor antagonist, over a period which included the time of implantation (late Day 5 to early Night 5), increased the number of blastocysts recovered from the uterus and reduced the number and intensity of Pontamine Sky Blue (PSB) sites obtained at autopsy on Night 5. Histological examination of the PSB sites taken on Night 5 from animals receiving the histamine antagonists revealed that the stromal oedema, which is characteristic of the attachment phase of pregnancy, had been inhibited.

Animals↗
PubMed1983

Histamine release into tracheal lumen and bronchial reactivity. Effect of compound 48/80 administered by different routes in various doses on histamine release and bronchial reactivity.

The influence of tracheal lavage with compound 48/80 on the bronchial response to challenge with ACH and AE was studied in 24 animals. Furthermore, the effect of i.v. administration of 48/80 was compared to its administration into the tracheal lumen. No increased histamine liberation was detected in the tracheal fluid after lavage with 48/80, nor was an influence on the bronchial response observed. These observations were the same as those described for tracheal lavage with water. The same amounts of this secretagogue induced, after i.v. administration, a high histamine release which correlates significantly with blood pressure decrease.

Acetylcholine↗
PubMed1988

Pathophysiological significance of the distribution of histamine receptor sub-types: a proposed dual role for histamine in inflammation and type I hypersensitivity reactions.

The pathophysiological significance of histaminergic receptors located on the membranes of immunocompetent cells is reviewed. H2-receptor agonists decrease the immunological histamine release from isolated serosal mast cells and from isolated hearts taken from actively sensitised guinea-pigs. Histamine and H2-receptor agonists inhibit the generation of superoxide anion from human neutrophils activated by FMLP and by substance P. These observations lend further support to the hypothesis of an immunodepression exerted by the activation of H2-receptors, which can be converted to immunostimulation by treatment with H2-receptor antagonists.

Animals↗
PubMed1988

Dimethyl sulfoxide decreases the fluorescence yield of the reaction between histamine and ortho-phthalaldehyde and may influence histamine release.

A sensitive method for quantifying histamine is the assay based on the fluorescence of the product obtained after reacting the amine with ortho-phthalaldehyde. The presence of dimethyl sulfoxide (DMSO) even in concentrations as low as 1% decreases the yield of fluorescence. Neglecting this quenching leads to the erroneous conclusion that DMSO in a concentration dependent manner inhibits the thapsigargin induced histamine release from peritoneal rat mast cells. Apart from the release induced by the selective calcium ion mobilizers thapsigargin and ionophore A23147, DMSO potently inhibits the response to other secretagogues.

Aldehydes↗
PubMed1994

Histamine and tele-methylhistamine in cat plasma after intravenous injection of histamine.

The effects of increased plasma histamine (Hi) on plasma tele-methylhistamine (MeHi) levels and the kinetics of Hi and MeHi elimination from plasma were studied in the cat. Hi (40 or 50 micrograms/kg) was injected intravenously and then Hi and MeHi were assayed by HPLC. Hi injection was followed by a significant increase in plasma MeHi levels, being maximal at 2-4 min. In most animals, maximal MeHi levels exceeded Hi itself. The half-lives (t1/2) of injected Hi were 0.6 and 13.3 min (mean values) in the alpha- and beta-phases, while the corresponding values for MeHi were 1.1 and 15.4 min. The t1/2 of exogenous MeHi (64 micrograms/kg, i.v.) was in the same range. Inhibitors of histamine-N-methyltransferase diminished the elimination rate of both amines studied. Plasma MeHi can thus serve as a marker for increased plasma Hi in the cat particularly because of its noticeable and delayed elevation after the rise in Hi itself.

Animals↗
PubMed1983

A new radioenzymatic assay for histamine using purified histamine N-methyltransferase.

Radioenzymatic assays for histamine (Hm) have found wide application. However, these procedures may lack the sensitivity necessary to quantify Hm in certain biological samples, such as human plasma. Purification of histamine N-methyltransferase (HNMT) has permitted the development of a new and highly sensitive radioenzymatic assay for Hm. HNMT was purified by sequential ion exchange, hydrophobic and molecular exclusion chromatography. The use of purified HNMT in the Hm assay has allowed the inclusion of high specific activity tritiated S-adenosyl-L-methionine ([3H]SAME) and the development of a simplified solvent extraction product isolation procedure. This assay has a sensitivity of approximately 2 picograms and is specific for Hm. Hm was easily quantified in human plasma and was found to be 303 +/- 81 pg/ml (mean +/- SD) in 8 male subjects. Substantial blank reduction and increased product conversion occur when purified HNMT is utilized in the Hm radioenzymatic assay, thus, increasing the sensitivity and possibly improving the specificity of this procedure.

Animals↗
PubMed1986

Histamine and histamine receptors: behavioral thermoregulation in the salamander Necturus maculosus.

Low doses (0.01, 0.1 mg/kg, i.p.) of histamine (HA) caused selection of significantly lower temperatures, and higher doses (0.5, 1.0 mg/kg) increased temperatures by mudpuppies in linear thermal gradients. Injection of the HA precursor, L-histidine (500 mg/kg) produced an increase in the temperatures selected. Results from injections of HA H1-receptor agonist (2-pyridylethylamine) and antagonist (pyrilamine), and H2-receptor agonist (dimaprit) and antagonist (cimetidine) had significant effects on thermoregulation; H1-receptors may mediate behavioral hyperthermia and H2-receptors behavioral hypothermia. Responses to these histaminic compounds are significantly influenced by the time of day at which the responses are measured and by season and acclimation temperature. The equivalent behavioral responses in both endotherms and ectotherms to agents which produce physiological hyperthermia and hypothermia are probably behavioral hypothermia ("cold seeking") and behavioral hyperthermia ("heat seeking"), respectively.

Animals↗
PubMed1995

Histamine H1 receptor occupancy in human brains after single oral doses of histamine H1 antagonists measured by positron emission tomography.

1. Histamine H1 receptor occupancy in the human brain was measured in 20 healthy young men by positron emission tomography (PET) using [11C]-doxepin. 2. (+)-Chlorpheniramine, a selective and classical antihistamine, occupied 76.8 +/- 4.2% of the averaged values of available histamine H1 receptors in the frontal cortex after its administration in a single oral dose of 2 mg. Intravenous administration of 5 mg (+)-chlorpheniramine almost completely abolished the binding of [11C]-doxepin to H1 receptors (H1 receptor occupancy: 98.2 +/- 1.2%). 3. Terfenadine, a nonsedative antihistamine, occupied 17.2 +/- 14.2% of the available H1 receptors in the human frontal cortex after its administration in a single oral dose of 60 mg. 4. There was no correlation between H1 receptor occupancy by terfenadine and the plasma concentration of the active acid metabolite of terfenadine in each subject. 5. PET data on human brain were essentially compatible with those on H1 receptor occupancy in guinea-pig brain determined by in vivo binding techniques, although for the same H1 receptor occupancy the dose was less in human subjects than in guinea-pigs. 6. The PET studies demonstrated the usefulness of measuring H1 receptor occupancy with classical and second-generation antihistamines in human brain to estimate their unwanted side effects such as sedation and drowsiness quantitatively.

Administration, Oral↗
PubMed2006

Recent advances in molecular pharmacology of the histamine systems: physiology and pharmacology of histamine H3 receptor: roles in feeding regulation and therapeutic potential for metabolic disorders.

Histamine H3 receptors (H3Rs) are autoreceptors that negatively regulate the release of histamine and other neurotransmitters such as norepinephrine, dopamine, and acetylcholine in the central nervous system (CNS). Consistent with the wide-spread projection of histaminergic neurons from the lateral hypothalamus, H3Rs are widely distributed in the CNS and are believed to play a variety of physiological roles, including regulation of feeding, arousal, cognition, pain, and endocrine systems. To further understand the physiological roles of H3Rs in vivo, we produced H3R knockout (H3R-/-) mice and found that H3R-/- mice displayed hyperphagia and late-onset obesity associated with hyperinsulinemia and leptinemia, the fundamental marks of metabolic syndromes. A series of non-imidazole H3R antagonists/inverse agonists with improved selectivity and potency have been developed and were found to regulate feeding and body weight gain in laboratory animals. Taken together, these observations suggest that H3Rs are involved in the regulation of feeding behavior and body weight. Several H3R inverse agonists targeting cognitive disorders and dementia have entered clinical trials. These trials will give critical information about the physiological functions of H3Rs in humans.

Animals↗
PubMed1992

Histamine analogues. 36th communication. Basically substituted histamine derivatives with H1-agonistic activity.

Piperidinoalkyl-, morpholinoalkyl- or [(pyrid-2-yl)methylthio]alkyl-substituents were introduced into position 2 of the essential histamine structure. These 2-substituted histamine derivatives were prepared via reaction of imidate hydrochlorides in liquid ammonia under pressure with 1,3-dihydroxypropanone followed by a stepwise build-up of the side chain in position 4 of the imidazole nucleus (route I) or by cyclization with 2-oxo-4-phthalimido-1-butyl acetate (route II) followed by deprotection of the primary amine function. The novel compounds were screened for H1-activity on the isolated guinea-pig ileum and for H2-activity on the isolated guinea-pig right atrium. While 10a, c-e proved to be weak partial H1-agonists, 10b, f were very weak H1-antagonists.

Animals↗
PubMedDate not supplied

Changes in the rat brain histamine content following metoprine and other histamine-methyltransferase (HMT) inhibitors.

Four compounds: amodiaquine, quinacrine, 1,4-(tele)-methylhistamine and metoprine, which in vitro effectively inhibit histamine N-methyltransferase (HMT) activity, were tested for their effects on histamine (HI) levels in the rat brain and ex vivo HMT activity. In in vitro studies all these compounds at concentration of 10 microM produced complete inhibition of HMT activity. Amodiaquine, quinacrine and 1,4-(tele)-methyl-HI weakly inhibited HMT activity ex vivo and they failed to alter HI levels in the rat brain. Of the tested compounds only metoprine significantly increased brain HI levels in both normal rats and 1-histidine treated rats. Metoprine and, to much lesser degree, amodiaquine, but not aminoguanidine, slowed down the disappearance of exogenous HI from the rat brain. It is suggested that metoprine, because of its simultaneous capability of inhibiting HMT activity and increasing brain HI level, might be a useful pharmacological tool in studies of HI metabolism and neurotransmission in the central nervous system.

Amodiaquine↗
PubMed1980

Effect of amodiaquine on histamine level and histamine-methyltransferase activity in the rat brain.

Amodiaquine, 10(-5) M, totally inhibited the activity of histamine-methyltransferase (HMT) in the rat brain. Both peripheral (60 mg/kg i.p.) and central (50 and 100 microgram i.vt.) administration of the drug substantially reduced the HMT activity. Amodiaquine given i.p. or i.vt., in various doses, did not change the endogenous histamine (HI) level in the rat brain at any time studied (1-24 h). Amodiaquine (60 or 120 mg/kg i.p.) administered together with an inhibitor of diamine oxidase, i.e. aminoguanidine (either peripherally or centrally) had no effect on the endogenous HI content. Possible involvement of mechanisms other than methylation or oxidation in regulation of the endogenous HI level in the rat brain is discussed.

Amine Oxidase (Copper-Containing)↗
PubMed1977

Phosphopyridoxal complexes with histamine and histidine. (5) The kinetics of cyclic compound formation between histamine and pyridoxal-5'-phosphate in the presence of pig kidney diamine oxidase and rat intestinal histaminase.

Pig kidney diamine oxidase (DAO) and rat intestinal histaminase (Hi-ase) activities are inhibited in vitro by high concentrations of both a substrate (histamine) and a coenzyme (pyridoxal-5'-phosphate). This inhibition may be at least partially associated with the formation of a cyclic compound between histamine (Hi) and pyridoxal-5'-phosphate (PLP). The dynamics of this cyclic compound formation in the presence of both enzymes has been examined. In an incubation mixture containing partially purified pig kidney DAO, the rate of cyclization decreased slightly as compared with a buffer. On the contrary, in the presence of crude rat intestinal histaminase, the rate of cyclization was inhibited significantly; this inhibition was proportional to the amount of enzyme preparation present in the incubation mixture. The possible mechanism of the influence of enzyme protein on the rate of cyclic compound formation, and its possible biological significance, are discussed.

Amine Oxidase (Copper-Containing)↗
PubMed1986

Histamine release by free radicals: paracetamol-induced histamine release from rat peritoneal mast cells after in vitro activation by monooxygenase.

The incubation of paracetamol with isolated rat serosal mast cells evokes the release of histamine only in the presence of (S10) liver microsomes obtained from PCB or phenobarbital treated rats. The release of histamine was not accompanied by a leakage of lactate dehydrogenase and was blocked by the antioxidant alpha-tocopherol and by D-mannitol, an hydroxyl free radicals scavenger. The data are consistent with the metabolic oxidation of paracetamol in the generation of reactive intermediates capable of activating the sequential exocytosis.

Acetaminophen↗
PubMed1988

Age dependent normal values of histamine and histamine metabolites in human urine.

We collected morning urine samples from normal healthy persons, who had not yet breakfasted, in the age range of 2-61 years and measured urinary excretion of histamine and its metabolites N tau-methyl-histamine and N tau-methylimidazoleacetic acid. The values obtained (expressed in terms of urinary creatinine excretion), were age dependent up to the age of 12. Thereafter, values stabilized and were no longer age dependent.

Adolescent↗