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At least 433 records · Page 24Linked to original sources
PubMed1993

In vitro cardiac pharmacology of the new histamine H2-receptor agonist amthamine: comparisons with histamine and dimaprit.

The cardiac activity of the novel histamine H2-receptor agonist amthamine was investigated in a variety of isolated heart preparations from guinea pigs and humans and in the isolated rabbit aorta. Amthamine caused an increase in the sinus rate of spontaneously beating guinea-pig atria (pD2 = 6.72) and in the contractility of the electrically driven guinea-pig papillary muscle (pD2 = 6.17) and of the human atrium (pD2 = 5.38). In all these systems, amthamine behaved as a full agonist with a potency comparable to or slightly higher than that of histamine and 10 times higher than that of dimaprit. The positive effects of amthamine were competitively antagonized by ranitidine which had pA2 values (6.46 and 6.25 in the guinea-pig atria and papillary muscle, respectively) comparable with those calculated against histamine and dimaprit. In the isolated rabbit aorta amthamine was devoid of H1-mediated activities up to 3 x 10(-4) M. These results indicate that amthamine is a potent and selective histamine H2-receptor agonist which can be considered a valuable tool for investigating H2-receptor mediated effects in cardiac tissues.

Animals↗
PubMed1994

Inhibition of IgE- and non-IgE-mediated histamine release from human basophil leukocytes in vitro by a histamine H1-antagonist, desethoxycarbonyl-loratadine.

Loratadine, a new nonsedating histamine H1-antagonist, has been shown to inhibit immunologic release of inflammatory mediators in addition to its H1-receptor blocking properties. After oral administration, the agent is metabolized primarily to desethoxycarbonyl-loratadine (DCL). The basic piperidine, DCL, is readily soluble in water, whereas the nonbasic urethane, loratadine, is insufficiently soluble in water for some in vitro investigations. Therefore we used the metabolite, DCL, to study its influence on in vitro leukocyte histamine release (LHR) in 24 allergic and 22 nonallergic subjects. IgE-mediated and calcium ionophore A23187-induced LHR were inhibited by DCL in a dose-dependent fashion (values of drug concentration to induce 30% inhibition after stimulation with inhalant antigen, anti-IgE, concanavalin A, and calcium ionophore A23187 were 6, 8, 5, and 11 mumol/L, respectively). Higher concentrations of DCL caused mediator release in all subjects (n = 45, 30 mumol/L DC: 11% +/- 2% LHR, 100 mumol/L DCL: 35% +/- 1% LHR), abolishing any inhibitory effect of the drug. Rapid onset of inhibition by 10 mumol/L DCL was found in kinetic studies (n = 10). The inhibition of anti-IgE-induced histamine secretion was synergistically increased by simultaneous preincubation of DCL with the potent histamine H2-agonist, FRA-19. Additional data indicate that the inhibition of LHR by DCL might involve biochemical events that occur after cellular Ca++ influx because LHR induced by N-formyl-methionyl-leucyl-phenylalanine or the phorbol ester, 12-O-tetradecanoyl phorbol-12-acetate, was not significantly affected by DCL.

Basophils↗
PubMed1994

The selective histamine H1-receptor agonist 2-(3-trifluoromethylphenyl)histamine increases waking in the rat.

The effects of the selective histamine H1-receptor agonist, 2-(3-trifluoromethylphenyl)histamine, were studied in rats implanted with electrodes for chronic sleep recordings. 2-(3-Trifluoromethylphenyl)histamine (80-120 micrograms) injected into the left lateral ventricle increased wakefulness, whereas slow wave sleep was reduced. Pretreatment with pyrilamine (2.0 mg/kg) prevented the effects of the H1-receptor agonist on wakefulness and slow wave sleep. Our results further support the involvement of histamine in the modulation of the waking state.

Animals↗
PubMed1998

Radio-enzymatic determination of histamine: interference by fluoride and possible activation of histamine methyl transferase.

The reproducibility of a radio-enzymatic method for determining plasma histamine was found to be affected by the anti-coagulant used for collecting blood. Recovery experiments from whole blood indicated that heparin yielded values that were more accurate than with EDTA or sodium fluoride; fluoride gave a mean value which was +41% higher than with heparin (P=0.054). Addition of fluoride to a standard calibration curve, and of increasing amounts to aliquots of 5 ng histamine also yielded higher values than in controls, up to +15% (P<0.1) and +14.1% (P=0.03) respectively. Fluoride did not affect the detecting system and was not contaminated with histamine; nor did it breakdown the methyl donor, S-adenosyl-L-methionine. It is concluded that heparin is the anti-coagulant of choice and that fluoride may activate histamine methyl transferase from pig brain. Fluoride may possibly have a biological role as an enzyme-activator and a usefulness in the therapy of mastocytosis.

Edetic Acid↗
PubMed2003

Cyclopropane-based conformational restriction of histamine. (1S,2S)-2-(2-aminoethyl)-1-(1H-imidazol-4-yl)cyclopropane, a highly selective agonist for the histamine H3 receptor, having a cis-cyclopropane structure.

A series of cyclopropane-based conformationally restricted analogues of histamine, the "folded" cis-analogues, i.e., (1S,2R)-2-(aminomethyl)-1-(1H-imidazol-4-yl)cyclopropane (11), (1S,2S)-2-(2-aminoethyl)-1-(1H-imidazol-4-yl)cyclopropane (13), and their enantiomers ent-11 and ent-13, and the "extended" trans-analogues, i.e., (1R,2R)-2-(aminomethyl)-1-(1H-imidazol-4-yl)cyclopropane (12) and its enantiomer ent-12, were designed as histamine H(3) receptor agonists. These target compounds were synthesized from the versatile chiral cyclopropane units, (1S,2R)- and (1R,2R)-2-(tert-butyldiphenylsilyloxy)methyl-1-formylcyclopropane (14 and 15, respectively) or their enantiomers ent-14 and ent-15. Among the conformationally restricted analogues, the "folded" analogue 13 (AEIC) having the cis-cyclopropane structure was identified as a potent H(3) receptor agonist, which showed a significant binding affinity (K(i) = 1.31 +/- 0.16 nM) and had an agonist effect (EC(50) value of 10 +/- 3 nM) on the receptor. This compound owes its importance to being the first highly selective H(3) receptor agonist to have virtually no effect on the H(4) subtype receptor. These studies showed that the cis-cyclopropane structure is very effective in the conformational restriction of histamine to improve the specific binding to the histamine H(3) receptor.

Animals↗
PubMed1979

Effects of histamine, of histidine and of anti-histaminic agents on the release of glucagon and insulin from the rat pancreas.

We have studied the effect of histamine (HA) and histidine (HIS) on the release of immunoreactive glucagon (IRG) and insulin (IRI) by isolated rat islets and pieces of pancreas. In isolated islets, HA and HIS stimulated IRG release at a glucose concentration of 3.0 mg/ml and IRI release at a glucose concentration of 0.5 mg/ml. In pieces of pancreas incubated in the presence of glucose (3.0 mg/ml), HA at a 2mM concentration stimulated IRG release and had no effect on the release of IRI; however, when the concentration of HA was doubled (4 mM), an inhibition of IRI release could also be demonstrated. HIS was ineffective. Perphenazine and dexchlorpheniramine, two anti-histaminic agents, inhibited IRG and stimulated IRI release. These results indicate that histamine, whether endogenous or exogenous, directly stimulated IRG and inhibits IRI release and suggest that some of the in vivo effects of histamine, such as hyperglycemia and lipid mobilization, may be mediated, at least in part, by these endocrinologic effects.

Animals↗
PubMed1996

Histamine and the nasal vasculature: the influence of H1 and H2-histamine receptor antagonism.

The aim was to determine the effect of H1- and H2-receptor blockade on histamine-induced changes in nasal airways resistance and lavage protein concentrations. Normal subjects were pretreated with oral cetirizine or ranitidine in a double-blind and randomized manner. Measurements of the concentration of total protein and albumin in nasal lavage fluid together with nasal airway resistance were made before and after challenge. Any effect of treatment was assessed by comparing the areas under the time-response curves. In all nine subjects available for analysis histamine caused an immediate increase in all measurements. Ranitidine reduced the maximum increase in nasal airway resistance, but this effect was significant only in combination with certirizine. The increase in lavage total protein and albumin concentrations was almost completely abolished by cetirizine, whereas ranitidine had less effect. We conclude that the histamine H1-receptor has the greatest effect on changes in nasal vascular permeability induced by topical histamine, whereas the H2-receptor has the greatest effect on nasal obstruction.

Adult↗
PubMed1982

Budesonide and nasal mucosal histamine content and anti-IgE induced histamine release.

The possible mode of action of the recently demonstrated steroid effect on the immediate type allergic reaction has been studied. The influence of a topical steroid, budesonide, on the nasal mucosal histamine content and anti-IgE induced histamine release was studied in an open study. A 1-week treatment with budesonide, used locally in the nose, was administered to 22 hay fever patients who were studied out of the pollen season. There was a decrease of histamine content after steroid treatment and also a blockade of the anti-IgE mediated histamine release, as shown in an in vitro release procedure. This steroid effect may partly explain the effect of steroids on the immediate reaction, as it has been demonstrated in allergen challenge studies.

Adolescent↗
PubMed1973

Histamine H2-receptors modulate systemic anaphylaxis: a dual cardiovascular action of histamine in calves.

Depressor changes in carotid blood pressure caused by histamine or anaphylaxis in calves, were incompletely blocked by the H(1)-receptor antagonist mepyramine. Burimamide, the selective histamine H(2)-receptor antagonist, potentiated the depressor actions of histamine and anaphylaxis. Potentiated depressor responses were inhibited by mepyramine. Observations are consistent with histamine stimulating both H(1)- and H(2)-receptors to cause respectively vasodilatation and vasoconstriction.

Anaphylaxis↗
PubMed1975

Effect of amodiaquine on gastric histamine methyltransferase and on histamine-stimulated gastric secretion.

1 Amodiaquine was found to be a potent inhibitor in vitro of gastric histamine methyltransferase from human and canine corpus and from pig antrum. The ID50 for the enzyme, purified from pig antrum mucosa by ultracentrifugation and chromatography on DEAE-cellulose, was 2.5 muM. 2 In six dogs with Heidenhanin pouches the maximum secretory response to histamine (40 mug/kg i.m.) was augmented by i.m. injection of amodiaquine. The augmentation depended on the dose of amodiaquine, the optimum effect (40% increase in volume of gastric juice, 80% in acid output) being achieved with 2 mg/kg. The maximum secretory response to betazole was also enhanced by amodiaquine. 3 It was suggested that amodiaquine may enhance the histamine and betazole stimulated gastric secretion by an inhibition of gastric histamine methyltransferase in vivo.

Amodiaquine↗
PubMed1975

Interaction of histamine H1-and H2-receptor antagonists with histamine uptake and metabolism by guinea-pig isolated atrium and mouse neoplastic mast cells cells in vitro.

1. Burimamide, metiamide, chlorpheniramine, triprolidine and cocaine, were tested as inhibitors of histamine uptake and metabolism in the guinea-pig atrium and in mouse neoplastic mast cells. 2. Cocaine did not affect the uptake and metabolism of histamine, either in the atrium or in the mast cells. All the antihistamines tested blocked the uptake and metabolism of histamine in both preparations. The order of potency was burimamide greater than chlorpheniramine greater than triprolidine greater than metiamide in the atrium; and burimamide greater than metiamide greater than triprolidine greater than chlorpheniramine, in the mase cells. 3. Comparison of the present results with the antihistamine activity of these blocking agents suggests that no correlation exists between the receptor blocking activity and the ability of these substances to act as inhibitors of histamine uptake and metabolism.

Animals↗
PubMed1977

Tissue blood flow and distribution of cardiac output in cats: changes caused by intravenous infusions of histamine and histamine receptor agonists.

1 The effects of infusions of histamine on blood pressure, cardiac output, heart rate, total peripheral resistance, stroke volume and tissue blood flow have been determined in anaesthetized cats using radio-active microspheres to measure cardiac output and tissue blood flow.2 Histamine caused dose-dependent falls in blood pressure and total peripheral resistance over the dose-range 1 x 10(-8) to 3.3 x 10(-7) mol kg(-1) min(-1). Histamine had no effect on cardiac output, heart rate or stroke volume.3 Histamine caused vasodilatation in the heart and stomach, with increased blood flow through these organs, and in the small and large intestine where blood flow was maintained despite the falls in arterial blood pressure. Blood flow to the brain, kidneys, liver, adrenal glands, skeletal muscle, spleen and skin was reduced when arterial blood pressure fell. Vascular resistance increased in the skin and spleen, presumably due to reflex vasoconstriction when blood pressure fell.4 The selective H(1)-receptor agonist 2-(2-aminoethyl)pyridine lowered blood pressure and decreased total peripheral resistance but did not change cardiac output, heart rate or stroke volume. 2-(2-Aminoethyl)pyridine caused vasodilatation in the heart, small and large intestine and kidneys. Vascular resistance was increased in the spleen and skin.5 The selective H(2)-receptor agonist 4-methylhistamine also lowered blood pressure and decreased total peripheral resistance but did not change cardiac output, heart rate or stroke volume. 4-Methylhistamine caused vasodilatation in the heart, stomach, small and large intestines and skeletal muscle. Vascular resistance was increased in the skin.

Animals↗
PubMed1982

Neurotensin stimulates exocytotic histamine secretion from rat mast cells and elevates plasma histamine levels.

1. Neurotensin stimulated histamine release and granule extrusion when applied to isolated rat peritoneal mast cells. 2. This secretory response was prevented by the removal of calcium or energy and was not accompanied by the release of lactic dehydrogenase. 3. The secretory response produced by neurotensin was prevented by prior treatment of mast cells with cromoglycate. 4. The intravenous injection of neurotensin into anaesthetized rats produced a rapid and significant increase in the level of blood histamine that was dependent upon the dose of neurotensin. 5. Treatment of rats with compound 48/80, 24 hr before neurotensin, abolished the elevation in blood histamine caused by neurotensin. The intravenous injection of cromoglycate 1-2 min before neurotensin greatly reduced the response to neurotensin. 6. The intradermal injection of neurotensin (0.03-30 p-mole) increased capillary permeability in rats pre-treated intravenously with Evans Blue. This response was abolished by the antihistamine, diphenhydramine. Increasing the dose of neurotensin to 300 p-mole partially overcame this inhibition by diphenhydramine. 7. Our results demonstrate that neurotensin can elicit an exocytotic secretory response from isolated rat peritoneal mast cells and elevate histamine levels in blood. It is suggested that some of neurotensin's physiological effects may be due to stimulation of mast cell secretion.

Animals↗
PubMed1980

Biological variation in the immunological release of histamine from replicates of passively sensitized human lung and its relation to histamine content.

The histamine content of weighed replicates of chopped human lung was found to vary greatly. Replicates also varied considerably in the amount of histamine released after passive sensitization with IgE and challenge with antigen. The amount of immunological release of histamine was poorly related to tissue histamine content. Consequently, expression of release as percent of content did not lead to any decrease in the amount of variation between replicates.

Allergens↗
PubMed2006

Recent advances in molecular pharmacology of the histamine systems: roles of C-terminal tails of histamine receptors.

G-protein-coupled receptors (GPCR) represent a large and diverse superfamily of integral membrane proteins to which histamine receptors belong. Increasing numbers of proteins have been identified to interact with the C-termini of GPCRs. These interactions are implicated in targeting, trafficking, and fine-tuning of signaling of GPCRs. Although the C-terminus of the histamine H2 receptor has been suggested to play in agonist-induced internalization of the receptor, roles of the C-termini of the other three histamine receptors are not known. To date, there is no protein identified to interact with the C-termini of histamine receptors.

Endocytosis↗
PubMed1995

Histamine, histamine H2-receptor antagonists, gastric acid secretion and ulcers: an overview.

Histamine, a biogenic amine, is involved in allergic reactions and asthma. The involvement of histamine in peptide ulcers is reviewed here. The discovery, distribution, synthesis, catabolism, and pharmacological effects of histamine are briefly described. Histamine actions are mediated by more than one type of receptor. The discovery, development and mode of action of H2-antagonists is discussed. A brief comparison of the clinical profiles (dosage regimen, metabolism and drug interactions) of the four currently used H2-antagonists (cimetidine, ranitidine, nizatidine and famotidine) is given. Furthermore, due to their ability to bind to cytochrome P-450, these compounds have the potential to interfere with the hepatic clearance of other drugs which are also metabolised by the mixed-function oxidase system in man. Therefore, a brief discussion of their adverse effects and drug interactions is included. Modulation of gastric acid secretion, in particular the role of cAMP and the proton pump, is described. Peptic ulcer is a major disease in the Western world and the aetiology and treatment of peptic ulcer are summarised.

Animals↗
PubMed1999

Cardiotoxicity of histamine and the possible role of histamine in the arrhythmogenesis produced by certain antihistamines.

Since 1990 it has repeatedly been reported that some histamine H1 receptor antagonists (e.g. terfenadine and astemizole) are able to produce ventricular arrhythmias (e.g. torsade de pointes) when they are given at dosages above the therapeutic range and/or administered together with cytochrome P-450 3A4 inhibitors, such as ketoconazole or erythromycin. Although the mechanism by which these arrhythmias are produced remains unclear, the recently reported ability of these drugs to block outward K+ currents has been suggested as the cause of their arrhythmogenic effects. Alternatively, we have observed that some H1 antihistamines, including terfenadine and astemizole, are able to release histamine from guinea-pig cardiac mast cells. Thus, we have proposed that the liberated histamine, acting through an H2 receptor-stimulating mechanism, can prolong the action potential duration and hence induce arrhythmogenic effects. This paper describes experimental observations supporting the hypothesis that some H1 antihistamines can induce severe cardiac arrhythmias via the local release of histamine.

Animals↗
PubMed1986

[Histamine receptor-bearing lymphocytes. VI. Influence of histamine on the Go-G1 transition of activated lymphocytes].

Histamine (10(-4) M) suppressed the PHA-induced activation of lymphocytes in vitro. This was shown by inhibition of the expression of DR- and 4F2-antigens, of the blast transformation, DNA- and RNA-synthesis, and the formation of thermostable sheep erythrocyte rosettes. Histamine affect these phenomenons only when added to the culture during the first hours. Already 6 hrs after addition of PHA, it exerted no significant suppression. The target of the inhibiting effect of histamine is the G0-G1-transition of the lymphocytes. Cells that already had entered the G1-phase were no more susceptible to histamine.

Animals↗