Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HISTAMINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 253 records · Page 14Linked to original sources
PubMed1990

Histamine acting on a histamine type 1 (H1) receptor increases beta-glucuronidase release from human lung macrophages.

The effects of histamine on lung macrophages have been studied by both biologic and radioligand experiments. After overnight adherence, lung macrophages spontaneously released beta-glucuronidase (beta-G) at a rate of approximately 7 nmol of hydrolyzed substrate/h/million cells. Histamine at low concentrations (10(-9) to 10(-8) M) resulted in a consistent potentiation of this release. The concentration-effect curve of histamine was bell-shaped, reaching an optimum at 10(-9) M, with concentrations greater than 10(-8) M having no significant effect. At a maximally effective concentration (10(-9) M), histamine evoked a 135 +/- 9.6% (mean +/- SE; n = 8, P less than 0.001) potentiation in the total amount of beta-G released during the first 60 min of incubation. This increase in beta-G release represented both a slight increase in beta-G synthesis as well as an increase in the percentage of beta-G released. When the secreted beta-G is expressed as a percentage of total content, histamine (10(-9) M) evoked a 125 +/- 3.2% (mean +/- SE; n = 27, P less than 0.0005) enhancement. The potentiation of beta-G release by histamine was evident after 45 min of incubation and persisted for up to 6 h. The potentiation of beta-G by histamine was sensitive to inhibition by pyrilamine (10(-7) M).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Differential inhibition of human liver phenacetin O-deethylation by histamine and four histamine H2-receptor antagonists.

1. The effects of histamine and four histamine H-2 receptor antagonists on phenacetin O-deethylation by microsomal preparations of four human livers was quantified by a radiometric-thin layer chromatographic method. 2. Histamine and three of these drugs, namely cimetidine, ranitidine and famotidine, were weak inhibitors of this cytochrome P-450-catalysed O-deethylation, but mifentidine was a potent competitive inhibitor with a Ki in the range 40-70 microM. 3. Cimetidine, histamine and mifentidine are all 4(5)-substituted imidazole derivatives, and the contrast between the very weak inhibitory effects of cimetidine and histamine, and the more potent effect of mifentidine, suggests that the imidazole moiety may play little role in the inhibition of phenacetin O-deethylase by mifentidine. 4. The demonstration that cimetidine, ranitidine and histamine were all poor inhibitors of phenacetin oxidation further suggests the possible lack of identity between the human liver cytochrome P-450 isoenzymes responsible for catalyzing the oxidation of metoprolol and phenacetin. This follows from recognizing that metoprolol oxidation is known, from both in vivo and in vitro studies, to be strongly inhibited by both of these H-2 receptor antagonists and from in vitro studies also to be inhibited by histamine.

Binding Sites↗
PubMed1992

Histamine N-methyltransferase controls the contractile response of guinea pig trachea to histamine.

The contractile response of isolated guinea pig trachea to histamine was potentiated in the presence of the histamine N-methyltransferase (HMT) inhibitor SKF 91488, whereas the diamine oxidase inhibitor aminoguanidine was without effect. SKF 91488 shifted in a concentration-dependent fashion the concentration-response curves to histamine to lower concentrations with the maximum by 1 log unit. The trachea contained significant HMT activity (45.4 +/- 5.0 pmol/min/mg protein). In situ hybridization to detect HMT mRNA indicated that HMT mRNA was present in the epithelium and endothelium, being more abundant in the former. Removal of the epithelium shifted the concentration-response curves to histamine to lower concentrations by 0.8 log unit, and SKF 91488 caused only a slight shift of histamine concentration-response curves in tissues denuded of epithelium. These findings suggest that HMT regulates the contractile response of guinea pig trachea to histamine, and epithelial removal-induced bronchial hyperresponsiveness to histamine is largely explained by the loss of HMT in the epithelium.

Animals↗
PubMed1985

Effects of histamine and a histamine releaser on body temperature and blood levels of metabolites and thyroid hormones in the pigeon.

Intravenous injections of histamine (20-600 micrograms) as well as of compound 48/80 (10-100 micrograms), a histamine releaser, produced a significant drop in the cloacal temperature of pigeons when examined during the initial 2 hr period following the injections. The effect of histamine was dose-dependent. A trend towards a drop in foot temperature was indicated with higher doses of histamine, but no effect was seen with compound 48/80. Plasma free fatty acid (FFA) levels were significantly increased at 15 and 30 min post-injection of histamine but an increase with compound 48/80 was obtained only at 15 min. While histamine produced a hyperglycaemic effect that was significant only at 30 min post-injection, compound 48/80 showed no such effect. Histamine caused a significant drop in the plasma levels of thyroxine (T4) and triiodothyronine (T3) both at 15 and 30 min post-injection. A similar trend in the thyroid hormone levels was also produced by compound 48/80, except for the T4 level at 15 min post-injection which showed no change.

Animals↗
PubMedDate not supplied

Epithelium-dependent relaxation of guinea-pig tracheal smooth muscle by histamine: evidence for non-H1- and non-H2-histamine receptors.

Epithelium-dependent modulation of the effect of histamine on airway smooth muscle of guinea-pig was studied by using the coaxial bioassay system. Histamine-induced contraction was followed by epithelium-dependent relaxation in the presence of indomethacin, propranolol, atropine and cimetidine. Mepyramine failed to prevent histamine-induced epithelium-dependent relaxation of carbachol-precontracted tracheal smooth muscle in the presence of cimetidine. This relaxant response could be prevented by an H3-histamine receptor antagonist, thioperamide. An agonist, (R) alpha-methylhistamine, of novel (H3)-histamine receptors was found ineffective to produce epithelium-dependent relaxation. It is concluded that the stimulation of non-H1- and non-H2-histamine receptors of guinea-pig airway epithelial cell layer takes part in the release of (a) relaxant factor(s), which counteracts, H1-histamine receptor-mediated bronchoconstriction.

Animals↗
PubMed1975

Cardiac histamine-ouabain interaction: potentiation by ouabain of the arrhythmogenic effects of histamine.

Cardiac effects of histamine include stimulation of sinus rate and ventricular contractile force, impairment of atrioventricular conduction and increase in ventricular automaticity. Atrioventricular block and increase in ventricular automaticity are common features of digitalis toxicity. The purpose of the present investigation was to study the influence of low concentrations of ouabain on the cardiac effects of immunologically released and administered histamine. Hearts excised from guinea pigs passively sensitized to penicillin antigens responded to antigen with sinus tachycardia, atrioventricular conduction block, increase in ventricular automaticity, decrease in coronary flow rate and histamine release. During anaphylaxis in the presence of ouabain, 10-9 and 3 times 10-9 M, the duration of conduction arrhythmia and the incidence of ventricular automaticity were greatly increased. Dose-response studies for the cardiac effects of exogenous histamine were conducted in vitro in the presence of ouabain 10-9 and 3 times 10-9 M. Ouabain, in a concentration-dependent fashion, potentiated histamine-induced prolongation of the P-R interval, but not the increases in sinus rate and in ventricular contractile force. Oution block and idioventricular also greatly increased the incidence of histamine-induced atrioventricular conduction block and idioventricular rhythms. Our results clearly identify a histamine-Ouabain interaction leading to severe disruption of atrioventricular conduction and to increased ventricular automaticity.

Animals↗
PubMed1976

Histamine release from cultured human basophils: lack of histamine resynthesis after antigenic release.

Human peripheral basophils can be maintained in cultured for up to 72 hr. These cells retain their functional integrity as judged by total histamine content and by their ability to release histamine by an IgE-mediated reaction in response to a specific antigen challenge. Cells cultured after suboptimal antigenic challenge could be activated to release histamine upon the addition of antigen. In contrast, cells culture after supra-optimal antigenic challenge did not fully recover their ability to release histamine even after 24 hr. With a variety of culture conditions, it was impossible to demonstrate any net synthesis of histamine in cells. Cells cultured after depletion of their stores by reaction with antigen did not show any net histamine formation. The experiments suggest that the basophil in peripheral blood is functionally an end-stage cell and can participate in the histamine release reaction only once.

Antigens↗
PubMed2003

Improgan antinociception does not require neuronal histamine or histamine receptors.

Improgan, a chemical congener of the H(2) antagonist cimetidine, induces antinociception following intracerebroventricular (i.c.v.) administration in rodents, but the mechanism of action of this compound remains unknown. Because the chemical structure of improgan closely resembles those of histamine and certain histamine blockers, and because neuronal histamine is known to participate in pain-relieving responses, the antinociceptive actions of improgan were evaluated in mice containing null mutations in the genes for three histamine receptors (H(1), H(2), and H(3)) and also in the gene for histidine decarboxylase (the histamine biosynthetic enzyme). Similar to earlier findings in Swiss-Webster mice, improgan induced maximal, reversible, dose-related reductions in thermal nociceptive responses in ICR mice, but neither pre-improgan (baseline) nor post-improgan nociceptive latencies were changed in any of the mutant mice as compared with wild-type controls. Improgan also had weak inhibitory activity in vitro (pK(i)=4.7-4.9) on specific binding to three recently-discovered, recombinant isoforms of the rat H(3) receptor (H(3A), H(3B), and H(3C)). The present findings strongly support the hypothesis that neuronal histamine and its receptors fail to play a role in improgan-induced antinociception.

Analgesics↗
PubMed2000

Histamine H(2) receptors mediate the inhibitory effect of histamine on human eosinophil degranulation.

The effect of histamine on human eosinophil degranulation and the receptor mediating such effect were studied in vitro using the complement C5a-mediated eosinophil peroxidase (EPO) release model. Following pre-treatment with 5 microg ml(-1) cytochalasin B(CB), C5a induced a concentration-dependent release of EPO from eosinophils isolated from healthy donors. Histamine (0.1-50 microM), but not L-histidine, inhibited concentration-dependently C5a-induced EPO release with IC(50) (95% CI) of 0.6 microM (0.3-1.2 microM) and maximal inhibition of approximately 60%. A similar effect was seen with the selective H(2) agonists dimaprit (IC(50) (95% CI)=6.9 microM (3.2-10.6 microM)) and amthamine (IC(50) (95% CI)=0.4 microM (0.2-0.7 microM)). Neither the selective H(1) agonist 6-(2-(4-imidazolyl)ethylamino)-N-(4-trifluoromethylphenyl) heptanecarboxamide(HTMT), nor the selective H(3) agonists imetit (up to 100 microM) had any significant effect. The inhibition by histamine was reversed by cimetidine (0.1-30 microM) and other H(2) antagonists, but not the H(1) antagonist mepyramine (1.0- 100 microM), nor the H(3) antagonist thioperamide (1.0-100 microM). Cimetidine (1-30 microM) shifted to the right the dimaprit log dose-response curve, producing a pA(2) value of 5.9 and Schild's plot slope of 0.98, thus confirming simple competitive antagonism. Histamine (10-100 microM) increased intracellular level of adenosine 3',5'-cyclic monophosphate, which was completely abolished by cimetidine (30 microM), but not mepyramine or thioperamide. The cyclic AMP analogue - dibutyryl cyclic AMP - also inhibited degranulation (IC(50) approximately 300 microM). The cyclic AMP phosphodiesterase(PDE) IV inhibitor rolipram (10 microM) synergistically enhanced the inhibition of EPO release by histamine. These results suggest that histamine, via stimulation of H(2) receptors and a consequent elevation of intracellular levels of cyclic AMP, inhibits human eosinophil degranulation.

Adenylyl Cyclases↗
PubMed2004

Desloratadine inhibits constitutive and histamine-stimulated nuclear factor-kappaB activity consistent with inverse agonism at the histamine H1 Receptor.

BACKGROUND: The human histamine H1 receptor is constitutively active and exhibits basal activation of nuclear factor-kappaB (NF-kappaB), an important modulator of allergic inflammation. Certain H1 antihistamines have recently been shown to inhibit basal NF-kappaB activity by stabilizing the H1 receptor in an inactive state, a phenomenon called 'inverse agonism'. METHODS: We evaluated the effect of the new H1 antihistamine, desloratadine, on basal and histamine-stimulated NF-kappaB activity and compared it with the activities of other H1 antihistamines. RESULTS: Transiently transfected COS-7 cells co-expressing NF-kappaB-luciferase and the H1 receptor exhibited constitutive NF-kappaB activity. H1 antihistamines reduced basal NF-kappaB activity (rank order of potency: desloratadine > pyrilamine > cetirizine > loratadine > fexofenadine). Histamine stimulated basal NF-kappaB activity 8-fold, which was blocked by H1 antihistamines (rank order of potency: desloratadine > cetirizine > pyrilamine > loratadine > fexofenadine). Neither histamine nor antihistamines had any effect on NF-kappaB activity in the absence of the H1 receptor. CONCLUSIONS: Desloratadine, acting through the histamine H1 receptor, inhibited basal NF-kappaB activity and can thus be classified as an inverse agonist. Inhibition of basal and histamine-stimulated NF-kappaB activity may help to explain previously reported inhibitory effects of desloratadine on allergic inflammatory mediators.

Animals↗
PubMed1979

Cutaneous vascular histamine H1 and H2 receptors in the guinea-pig: the histamine skin wheal as a cutaneous vascular model.

The roles of histamine H1 and H2 receptors in histamine skin wheals were studied in the guinea-pig. Intradermal injections of histamine, 0.125--2 micrograms/0.1 ml, produced wheals in a dose dependent manner. Pyrilamine maleate (3.2 mg/kg p.o., pretreatment for 1 hour) produced a dose dependent shift of the histamine wheal dose-response curve to the right in a parallel fashion. Metiamide, 3, 10 or 30 mg/kg p.o., had no effect on the histamine dose-response curve. However, a combination of metiamide (10 or 30 mg/kg) and pyrilamine (3.2 mg/kg) further increased the effect of pyrilamine. It is concluded that both H1 and H2 receptors are involved in histamine-induced wheals in the guinea-pig.

Animals↗
PubMedDate not supplied

Inhibition of histamine-stimulated increases in heart rate in man with the H2-histamine receptor antagonist cimetidine.

The influence of an H2-histamine receptor antagonist, cimetidine, on histamine-induced changes in heart rate and blood pressure was examined in a randomized double-blind study in six fasted male subjects. The intravenous infusion of histamine (10 microgram/min) for 20 minutes caused an immediate and sustained increase in heart rate (26 per cent and a transient fall in mean arterial blood pressure (10 per cent). Cimetidine pretreatment (300 mg intravenously) inhibited histamine-elevated heart rate by 75 per cent (P less than 0.05) and histamine-decreased blood pressure by 54 per cent (P less than 0.05). Cimetidine by itself did not cause significant changes in heart rate or blood pressure. These results illustrate that H2-histamine receptor antagonists significantly inhibit histamine-induced increases in heart rate in man and support the potential use of cimetidine in certain cases of tachyarrhythmia.

Adult↗
PubMed1977

Mechanism of histamine binding II: effect of alkali metal and alkaline earth cations on histamine binding to peptide H.

The association constants of histamine with Mg2+, Ca2+, Sr2+, and Ba2+ were determined in buffer solutions at constant pH using an ion selective electrode. These cations enabled histamine to bind to peptide H. A minimum cation binding concentration was required for histamine binding. A linear relationship existed between the minimum cation binding concentration and the log of the equilibrium constant for the histamine-cation complexes, indicating that the specificity of the alkaline earth cations in promoting histamine binding was due to the difference in their ability to complex with histamine. The monovalent cations, Nat, Kt, and Cst inhibited histamine binding to peptide H, with the extent of inhibition dependent on cation concentration. An ion-exchange mechanism or a conformation change in the peptide may account for the inhibition.

Barium↗
PubMed1983

The effect of prostaglandin E2 on histamine-stimulated calcium mobilization as a possible explanation for histamine tachyphylaxis in canine tracheal smooth muscle.

Isolated strips of canine tracheal smooth muscle rapidly lost their responsiveness to histamine when placed in a zero calcium Krebs buffer. Responsiveness to acetylcholine, however, was not rapidly lost, and following 120 min of incubation in zero calcium buffer with frequent washes, 10% of the contractile response still remained. The kinetics of each loss of response suggest that primarily a loosely bound source of calcium is mobilized by histamine and a more tightly bound source is mobilized by acetylcholine. Consistent with these data were the effects of the calcium antagonist verapamil. In normal calcium Krebs solution, dose-response curves to histamine were markedly reduced by verapamil while acetylcholine responses were relatively unaffected. In calcium depleted tracheal strips, indomethacin potentiated the calcium dose-response curve, determined by incremental readdition of calcium in the presence of histamine (10(-4) M), with comparatively little effect on the calcium dose-response curve in the presence of acetylcholine (10(-6) M). Also, in indomethacin pretreated tracheal strips, a reduction in the histamine-calcium dose-response curve could be produced by exogenous addition of 2.8 X 10(-9) M and 2.8 X 10(-8) M PGE2. In the acetylcholine-calcium responses there was a significant reduction only at 2.8 X 10(-8) M PGE2. These data suggest that histamine mobilizes primarily a loosely bound, possibly extracellular source of calcium necessary for contraction, and this histamine-stimulated calcium mobilization is sensitive to the effects of PGE2.

Acetylcholine↗
PubMed1983

Histamine symptoms and histamine metabolism in chronic granulocytic leukaemia.

Histamine metabolism was investigated in three patients with chronic granulocytic leukaemia (CGL) during symptoms suspected to be caused by histamine release. Plasma histamine levels were excessively high compared with periods when the patients were symptomless or with CGL patients without such symptoms. The patients seemed to be adapted to high plasma histamine levels as the symptoms were not typically systemic in nature, but rather localized phenomena like oedema and pruritus in the extremities. Also CGL patients without symptoms showed abnormally high plasma histamine concentrations, which were significantly related to the whole blood histamine concentration. The possibility must be considered that part of the plasma histamine increase is artificial due to rupture of the basophils during the blood collection procedure.

Basophils↗
PubMed1978

Histamine and pancreatitis: increase of plasma histamine levels in dogs with Pfeffer preparation and influence of aminoguanidine on the survival time.

Histamine release could be shown in 50% of the dogs suffering from acute haemorrhagic pancreatitis in Pfeffer's preparation. The survival time of these dogs was shorter by about 50% than that of animals without alteration of the plasma histamine levels. The powerful diamine oxidase blocker aminoguanidine diminished the incidence of severe pancreatitis in the dogs without influencing survival time. As in animals treated by saline histamine release could be shown in 50% of the aminoguanidine-treated dogs in which higher plasma histamine levels were determined than in saline-treated animals. The survival time of the dogs with histamine release, however, was not different from that of animals with normal plasma histamine levels throughtout the experiment. The actions of aminoguanidine in Pfeffer's preparation seemed to be rather complex. Contrasting effects on the development of pancreatitis and on histamine inactivation may have influenced the survival time in different directions.

Acute Disease↗
PubMed1987

Histamine release from mast cells of various species induced by histamine releasing factor from human lymphocytes.

The aim of our work was to investigate the effect of histamine releasing factor (HRF), produced in vitro by lymphocytes obtained from atopic and non-atopic asthmatics, on mast cells of various species (mouse - peritoneal mast cells, hamster and rat - peritoneal and pleural mast cells, guinea-pig - mesenteric and pulmonary mast cells). We found that human HRF is able to release histamine from the examined mast cell populations in a dose-dependent fashion. Mast cells from various species differed in their susceptibility to the action of HRF; rat pleural and guinea-pig mesenteric and pulmonary mast cells were the most susceptible, while mouse and hamster peritoneal mast cells - the least susceptible. The presence of 50% D2O in the medium significantly increased HRF-induced histamine release from rat mast cells, while the addition of phosphatidylserine did not change it. HRF-induced histamine release from guinea-pig mesenteric mast cells was not related to sensitization of these cells. We also compared histamine release from guinea-pig pulmonary and mesenteric mast cells induced by human HRF produced in vitro by lymphocytes obtained from atopic and non-atopic asthmatics. We have found that supernatant from atopic asthmatics lymphocyte cultures released significantly more histamine than supernatant from non-atopic asthmatics lymphocyte cultures. Our studies give evidence that human HRF acts across the species barrier and induces histamine release from mast cells of various species. The mechanism of HRF action on mast cells seems to be different from that of allergen.

Animals↗
PubMed1985

Effect on mast cell histamine of inhibiting histamine formation in vivo with alpha-fluoromethylhistidine.

An irreversible inhibitor of histidine decarboxylase, alpha-fluoromethylhistidine (FMH), was used to inhibit histamine formation by mast cells in vivo. Even at doses of FMH sufficient to reduce histamine formation more than 95%, the ability of mast cells to synthesize histamine recovered rapidly. It was possible, however, to sustain levels of histamine-forming activity below 10% of normal with continuous administration of FMH from subcutaneously implanted osmotic pumps. Administration of FMH under these conditions did not deplete significantly mast cell histamine but did prevent the increase in total mast cell histamine that occurs over 14 days and also prevented the reconstitution of mast cell histamine stores after depletion by treatment with polymyxin B.

Animals↗