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At least 379 records · Page 21Linked to original sources
PubMed1998

Histamine-induced calcium mobilization in single cultured cells expressing histamine H1 receptors: a relationship between its sensitivity and the density of H1 receptors.

Stimulation of histamine H1 receptors initiates the hydrolysis of phosphatidylinositides and results in the production of inositol (1, 4,5)-triphosphate and intracellular Ca2+ mobilization. Although the mechanism for signal transduction via the H1 recptor has been extensively investigated, little is known about the correlation between the sensitivity of histamine-induced Ca2+ mobilization and the density of H1 receptors in cultured cells. Cytosolic free Ca2+ concentration ([Ca2+]i) after stimulation by histamine was monitored in single CHO and rat C6-glioma cells stably expressed with H1 receptors and astrocytoma 1321N1 cells using the Ca2+-sensitive dye Indo-1 and dynamic single cell imaging techniques (ACAS 570 laser cytometer). Both of the H1 receptor-expressed CHO cells and C6-glioma cells were over 10 times more sensitive to histamine than astrocytoma 1321N1 cells in which H1 receptors were naturally present. The density of H1 receptors in the transfected cells was also more than 10-fold that of 1321N1 cells. In addition, inhibition of intracellular Ca2+-ATPase by thapsigargin elicited an increase in [Ca2+]i in H1 receptor-overexpessed cells and astrocytoma 1321N1 cells with similar sensitivity. These data suggest that the sensitivity of Ca2+ mobilization by histamine in these cells was correlatively augmented with the increase in the density of H1 receptors.

Animals↗
PubMed1988

[The amount of histamine released in vivo by hypnotics (thiopental, methohexital, propofol) studied by assays of plasma histamine].

Accidents observed during induction of anaesthesia are most often linked to non-specific histamine liberation. The sale of new hypnotics (Methohexital and Propofol), has brought the hope that their histamine-liberation potential would be lower. The study was done in patients who were at risk of histamine-liberation (atopics, drug allergies etc.). Two series of patients were studied after anti H1 and tranquilizer premedication. Histamine liberation by Propofol versus Thiopental as the inducer was studied in the first group. In the second, the combination was Methohexital versus Thiopental. In both series studied the new hypnotics Propofol and Methohexital did not release histamine non-specifically in atopics at risk. Neither clinical reactions non increase of histamineamia were seen. It is concluded that these two new drugs are safe.

Drug Hypersensitivity↗
PubMed1982

Presence of histamine and histamine-metabolizing enzyme in rat and guinea-pig microvascular endothelial cells.

Purified microvascular endothelial cell preparations from guinea-pig perirenal fat pad, heart ventricles and brain cortex were found to contain high histamine methyltransferase (HMT) activity (4, 3, 4.4 and 1.2 nmol of histamine methylated/hr/mg of protein, respectively). The microvascular cells appeared to be the major source of HMT activity in the whole fat pad but not in heart and brain cortex, where the enzyme was present in other cells. The myocyte, for example, was an additional source of HMT activity (1.0 U/mg of protein) in heart. The same preparations from rat had no detectable HMT activity (less than 0.1 U/mg of protein). In contrast to HMT, the second histamine-metabolizing enzyme, diamine oxidase, was found in the microvascular preparations from both species, usually at much higher activity than the parent tissue. All the endothelial cell preparations contained a small (0.1-0.6 microgram/g of tissue; 10-50 ng/mg of protein) pool of histamine which was resistant to the action of Compound 48/80, although the functional significance of this pool is unclear. Thus, in addition to the presence of serotonin- and catecholamine-degrading enzymes, the microvascular endothelium also contains histamine-inactivating enzymes.

Adipose Tissue↗
PubMed1978

A clinical study of concanavalin A-induced histamine release utilizing a single isotopic enzymatic assay of histamine.

Concanavalin A (Con A)-induced histamine release from cells of subjects with extrinsic asthma, intrinsic asthma or urticaria and normal individuals was examined utilizing a single isotopic enzymatic assay for histamine. Maximum histamine release by Con A occurred with 0.9 to 4.5 microgram/ml. The mean percentage of maximum histamine release by Con A from cells of donors with extrinsic asthma was 36(+/- 19.3)% while that from cells of normal individuals was 21.4(+/- 23.7)%. However, there was no significant difference between the two groups. The higher reactivity to Con A of cells from individuals with intrinsic asthma or urticaria was not observed compared to that of the normal group. The histamine release by Con A was not correlated with IgE level in the plasma (r = 0.35). It was observed that compound 48/80 inhibited the enzymatic reaction in the isotopic, enzymatic assay.

Asthma↗
PubMedDate not supplied

The effects of a new generation of H1 antihistamines (cetirizine and loratadine) on histamine release and the bronchial response to histamine in atopic patients.

The effects of two selective H1 receptor blockers, cetirizine and loratadine, in comparison with placebo, on basophil histamine release and the bronchial response to histamine were assessed. The studies were performed in a group of 18 patients with pollinosis and 22 with atopic asthma. Both tests were performed before and after medication. Histamine release from isolated basophils was evaluated by Shore's method using anti-IgE and pollen antigen as stimulants. The bronchial provocation tests were performed by Ryan's method. The results were expressed as PC20FEV1. It was shown that both drugs significantly inhibited basophil histamine release induced by anti-igE or specific allergen. It was also found that these drugs effectively reduced the bronchial response to histamine challenge. These findings confirm the beneficial clinical effect of a new generation of selective H1 blockers in the treatment of IgE-mediated allergic diseases, and also the possible role of these drugs in the therapy of atopic asthma.

Adult↗
PubMed1995

Haemophilus influenzae release histamine and enhance histamine release from human bronchoalveolar cells. Examination of patients with chronic bronchitis and controls.

Haemophilus influenzae (H. influenzae), Streptococcus pneumoniae (S. pneumoniae) and Branhamella catarrhalis (B. catarrhalis) are often found in the lower respiratory tract of patients with chronic bronchitis. Earlier studies have shown that bacteria induce mediator release from human basophils and parenchymal lung mast cells. In this study the capability of bacteria to trigger or potentiate histamine release from superficially located mast cells in the airway epithelium was studied in cell suspensions obtained by bronchoalveolar lavage in patients with chronic bronchitis (CB). In approximately half of the patients H. influenzae and Staphylococcus aureus (S. aureus) were found to trigger histamine release, whereas no response was obtained by S. pneumoniae or B. catarrhalis. The mediator release was caused by a non-IgE-dependent mechanism. At lower concentrations of H. influenzae causing no histamine release the bacterium was found to enhance IgE-mediated histamine release triggered by anti-IgE antibody. The synergy was more pronounced in patients with CB than in controls. Since H. influenzae is found in the lower respiratory tract of the patients but not in normal individuals, the infection here may via histamine release lead to harmful effects on the airways of importance for precipitation and exacerbation of chronic bronchitis.

Adult↗
PubMed1987

Presynaptic and postsynaptic effects of histamine and histamine agonists in the superior cervical ganglion of the rat.

Extracellular and intracellular recording techniques were used to study the effects of histamine and the histamine agonists [impromidine (IMP) and 2-thiazolylethylamine (2-TH)] on synaptic transmission in the superior cervical ganglion of the rat in vitro. At the concentrations employed (up to 10(-5) M) these compounds did not produce detectable effects on the electrical properties of the postsynaptic neurons. Histamine produced a dose-dependent reduction in the amplitude of the extracellularly-recorded presynaptic and postsynaptic compound action potential. The H2 receptor agonist impromidine reduced only the postganglionic compound action potential. Cimetidine, a specific H2 receptor antagonist, produced parallel shifts in the log dose-response curves for impromidine. Impromidine also reduced the average size of the evoked excitatory postsynaptic potential. The reduction of the mean amplitude of the excitatory postsynaptic potential was due to a decrease in the amount of acetylcholine (ACh) liberated by each preganglionic volley (mean quantal content, m) and a diminution in quantal size. The H1 receptor agonist, 2-TH produced a dose-dependent increase in the presynaptic and postsynaptic compound action potential and in m. The increase in m was not associated with changes in quantal size. The H1 antagonists, pyrilamine and promethazine, did not prevent facilitation of ganglionic transmission induced by 2-TH. It is concluded that histamine H1 and H2 receptors exist on preganglionic axons, or terminals in sympathetic ganglia of the rat. Activation of H1 receptors facilitates release of ACh whereas H2 receptor activation results in depressed release.

Action Potentials↗
PubMed2002

Effects of histamine H3 receptor agonist and antagonist on histamine co-transmitter expression in rat brain.

The histaminergic H3-receptor (H3R) controls histamine synthesis and release in the tuberomamillary nucleus. We evaluated the effects of stimulating or blocking of H(3)R on glutamate-decarboxylase 67 kDa (GAD-67) and galanin mRNA expression, two histamine co-transmitters.After in situ hybridization histochemistry (ISHH), we observed a colocalization of 100% between histidine decarboxylase (HDC) and GAD-67 or H3R and of 80 to 97% with galanin. Adult rats received an H3R agonist ((R)alpha-Methylhistamine) or antagonist (ciproxifan) and were sacrificed 1 or 3 hours later. Treatment effects on HDC, galanin and GAD-67 mRNA were studied by quantitative ISHH on serial sections. Treatment with the H3R agonist known to decrease histamine neuron activity initially reduced HDC and galanin gene expression but an inverse change, presumably reflecting a compensatory mechanism, was observed after 3 h on both markers. In contrast, the H3R antagonist known to activate histamine neurons, had opposite effects on the two markers, suggesting that co-transmitters are submitted to independent control mechanisms. Furthermore, GAD-67 mRNA levels were not significantly modified by these treatments.

Animals↗
PubMed1981

Histamine actions on activity of cultured hypothalamic neurons: evidence for mediation by H1- and H2-histamine receptors.

Tuberal hypothalamic tissue cultures were used to investigate the actions of histaminergic agents on neuronal activity using extracellular glass micropipettes. Histamine and H1- and H2-agonists were applied locally onto single active neurons by iontophoresis, while histaminergic antagonists were perfused through the bathing medium. Peri-event histogram and ratemeter analysis showed histamine to both excite and depress unit activity. Excitations were only antagonized by putative H1- and not H2-histamine antagonists, whereas inhibitions were antagonized by H2- and H2-antagonists. Dimaprit, a specific H2-agonist, elicited inhibitions of activity, while 2-(2-pyridyl)ethylamine, a putative H1-agonist, elicited both excitations and inhibitions. Two pharmacologically distinct populations of histamine receptors may exit in the hypothalamus: excitatory H2-receptors and inhibitory H2-receptors.

Animals↗
PubMed2000

Constitutive activity of the histamine H(1) receptor reveals inverse agonism of histamine H(1) receptor antagonists.

Transient expression of the wild-type human histamine H(1) receptor in SV40-immortalised African green monkey kidney cells resulted in an agonist-independent elevation of the basal levels of the second messenger inositoltrisphospate. Several histamine H(1) receptor antagonists, including the therapeutically used anti-allergics cetirizine, loratadine and epinastine reduced this constitutive histamine H(1) receptor activity. Inverse agonism, i.e., stabilisation of an inactive conformation of the human histamine H(1) receptor, may therefore be a key component of the anti-allergic mechanism of action of clinically used antihistamines.

Animals↗
PubMed2002

Development of a new class of nonimidazole histamine H(3) receptor ligands with combined inhibitory histamine N-methyltransferase activity.

In search of novel ways to enhance histaminergic neurotransmission in the central nervous system, a new class of nonimidazole histamine H(3) receptor ligands were developed that simultaneously possess strong inhibitory activity on the main histamine metabolizing enzyme, histamine N-methyltransferase (HMT). The novel compounds contain an aminoquinoline moiety, which is an important structural feature for HMT inhibitory activity, connected by different spacers to a piperidino group (for H(3) receptor antagonism). Variation of the spacer structure provides two different series of compounds. One series, having only an alkylene spacer between the basic centers, led to highly potent HMT inhibitors with moderate to high affinity at human histamine H(3) receptors. The second series possesses a p-phenoxypropyl spacer, which may be extended by another alkylene chain. This latter series also showed strong inhibitory activity on HMT, and in most cases, the H(3) receptor affinity even surpassed that of the first series. One of the most potent compounds with this dual mode of action is 4-(4-(3-piperidinopropoxy)phenylamino)quinoline (34) (hH(3), K(i) = 0.09 nM; HMT, IC(50) = 51 nM). This class of compounds showed high antagonist potency and good H(3) receptor selectivity in functional assays in guinea pig on H(1), H(2), and H(3) receptors. Because of low or missing in vivo activity of two selected compounds, the proof of concept of these valuable pharmacological tools for the supposed superior overall enhancing effect on histaminergic neurotransmission failed to appear hitherto.

Animals↗
PubMed1981

Effects of histamine and histamine antagonists on intestinal capillary permeability.

Steady-state lymph flow, blood flow, and lymph and plasma total protein concentration were measured in an autoperfused cat ileum preparation during the continuous infusion of histamine at venous pressures of 0, 10, 20, and 30 mmHg. The capillary osmotic reflection coefficients for total proteins and each protein fraction were estimated. In addition, the ileum was pretreated with an H1-receptor antagonist (diphenhydramine) or with an H2-receptor antagonist (cimetidine). The results suggest that histamine selectively increases the ileal vascular permeability to plasma proteins of a molecular radius up to 96 A. The H1-receptor antagonist did not alter the histamine-induced permeability changes but did block the observed initial vasodilation. The H2-receptor antagonist significantly reduced the permeability changes associated with histamine while having only a slight effect on the initial vasodilation. It is concluded that the activation of H1-receptors is predominantly associated with the initial vasodilation, whereas the H2-receptors are predominantly associated with permeability.

Animals↗
PubMed1983

Inhibition of phytohaemagglutinin-induced proliferation of human peripheral blood lymphocytes by histamine and histamine H1 and H2 agonists.

Histamine (10(-3)-10(-8) M) inhibits PHA-induced proliferation of human peripheral blood lymphocytes (HPBL). Inhibition is detected at low concentrations of PHA but is rarely observed at high PHA concentrations. The histamine type II (H2) receptor agonists dimaprit, impromidine and 4-methylhistamine (4MH) inhibit HPBL proliferation and the H2 antagonist, cimetidine, reverses histamine-induced suppression of HPBL proliferation. Lymphocyte proliferation is also inhibited by the H1 receptor agonists, 2-pyridylethylamine and 2-thiazoylylethylamine, but only at high concentrations (10(-3) and 10(-4) M). The H1 agonist 2-methylhistamine, suppresses PHA-induced proliferation of HPBL in analogous fashion to histamine. This effect is reversed by cimetidine but not by diphenhydramine suggesting that an H2 receptor interaction is involved.

Cell Division↗
PubMed1978

Effect of histamine methylation inhibitors on entry of 14C-histamine into brain.

Pretreatment of mice, rats and guinea pigs with inhibitors of histamine methylation, followed by systemic injection of 14C-histamine, results in a significant increase in brain 14C-histamine relative to controls. It is suggested that the histamine methylating enzyme participates in the blood-brain barrier to histamine.

Amodiaquine↗
PubMed1984

Effect of cimetidine and carbenoxolone on cysteamine-induced ulcers: a study of gastric mucosal histamine and histamine formation capacity in rat.

Cysteamine-induced ulcers in rat were used to study the effect of ulcer-healing agents with different modes of action on ulcer formation and mucosal histamine. Male Wistar rats were divided into 5 groups. Group I had cysteamine injection; group II had cimetidine followed by cysteamine injection; group III had carbenoxolone before cysteamine injection; group IV had carbenoxolone as group III and cimetidine and cysteamine injections; group V had saline injections (controls). In group I 20/29; group II 17/30; group III 15/29; and group IV 23/30 developed ulcers. No significant differences were found. No ulcers were found in group V. Comparison between all groups and controls showed an increase in gastric mucosal histamine and HFC. The increase in histamine was related to ulcer formation. Duodenal and oesophageal histamine did not change significantly. Gastric mucosal histamine and HFC were directly correlated.

Animals↗
PubMed1984

Studies on cutaneous vascular permeability in the rat: increases caused by histamine and histamine-like agents.

The pharmacology of histamine-induced increases in microvascular permeability has been studied in rat skin. Histamine caused dose-dependent increases in microvascular permeability, assessed as increases in extravascular albumin accumulation. The responses to histamine were inhibited in a dose-dependent manner by pretreatment with mepyramine and were not changed by cimetidine. 2-(2-Aminoethyl)pyridine also increased microvascular permeability whereas impromidine did not. These results suggest that H1-receptors and not H2-receptors are involved in the permeability response to histamine in rat skin. In contrast, dimaprit increased microvascular permeability and responses to dimaprit exceeded the maximum response to histamine. The response to dimaprit proved to be independent of H2 receptors and was consistent with an indirect response due to mast cell degranulation.

Animals↗
PubMed1986

Endotoxins release histamine by complement activation and potentiate bacteria-induced histamine release.

The histamine-releasing capability of bacterial lipopolysaccharides (LPS) was examined in human leukocyte suspensions. LPS alone did not release histamine, but it was found to enhance the histamine release caused by bacteria in basophils from persons sensitized to these bacteria. In the presence of serum, LPS was able to release histamine through complement activation. It is speculated that endotoxins reinforce release of histamine caused by bacteria in persons sensitized to these microorganisms, and a direct mediator release via complement activation might play a role in septic conditions.

Bacteria↗
PubMed1988

Food-induced histaminosis as an epidemiological problem: plasma histamine elevation and haemodynamic alterations after oral histamine administration and blockade of diamine oxidase (DAO).

In a randomized controlled trial, 30 pigs were orally treated with histamine (60 mg). In addition, half of the animals underwent a specific blockade of the enzyme diamine oxidase (DAO), which is the main histamine catabolising enzyme in the intestinal tract. Only these DAO-blocked animals exhibited severe clinical symptoms (e.g. hypotension, flush, vomiting) and, in parallel, showed tremendous elevations of plasma histamine levels of up to 160 ng/ml. 3 out of 15 animals in this group died within the experimental period. In contrast, the control animals neither exhibited plasma histamine levels above 5 ng/ml nor had any clinical reactions. These results contradict the current opinion that oral histamine intake in food is not clinically relevant, especially since many commonly used drugs are DAO-inhibitors and approximately 20% of our population take these drugs. Apart from drugs, some other factors (alcohol, spoilt food etc.) can also function via a blockade of DAO as an additional risk. DAO-blockade is therefore a real epidemiological problem. Evidence is presented here for the new disease concept: Food-Induced Histaminosis.

Amine Oxidase (Copper-Containing)↗