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PubMed1993

In vivo microdialysis measurement of histamine in rat blood effects of compound 48/80 and histamine receptor antagonists.

An in vivo microdialysis method combined with a highly sensitive HPLC method which was developed for the analysis of the mediators in the CNS has been applied to assay histamine concentrations in the blood. The technique was used to study the effects of compound 48/80 and histamine receptor antagonists on histamine release in the blood of rats. The mean basal level of histamine in the blood measured by in vivo microdialysis was 177.8 +/- 11.1 pmol/mL. This level was not affected significantly by intraperitoneal (i.p.) injection of saline, and remained at the constant level for at least 8 hr after injection of saline. After i.p. injection of histamine (0.5 mg/kg), histamine was quickly detected in the blood of the jugular vein. Moreover, because the recovered histamine in the dialysate is directly proportional to the free fraction in the blood, the in vivo microdialysis method of blood is a reliable method of examining histamine release into the blood. In our experiments, the histamine level in dialysates from rat jugular vein was markedly increased by compound 48/80 (2.0 mg/kg, i.p.), demonstrating the histamine release into the blood from mast cells. However, there was no increase in histamine concentration after an i.p. injection of histamine receptor antagonists, such as pyrilamine (2.0 mg/kg), d-chlorpheniramine (2.0 mg/kg), cimetidine (10 mg/kg), or thioperamide (10 mg/kg). Thus, the present results suggested that these histamine receptor antagonists might not have an influence on histamine release into the blood.

Animals↗
PubMed1986

Pharmacological investigation into the effects of histamine and histamine analogues on guinea-pig and rat colon in vitro.

The effects of histamine and specific histamine agonists has been examined on isolated longitudinal colon strips of guinea-pig and rat. Histamine and 2-pyridyl-ethylamine but not 4 methylhistamine produced a concentration-related contractile response in the guinea-pig colon. The H1-antagonist clemizole antagonized competitively the effect of histamine but the H2-antagonist ranitidine did not modify the dose-response curve to histamine in the guinea-pig colon. Atropine, hexamethonium, prazosin and propranolol failed to modify the contractile response to histamine. Tone induced with KCl in guinea-pig isolated colon was not modified by histamine agonists even in tissues pretreated with clemizole or ranitidine. Histamine and histamine analogues were without effect on the isolated longitudinal strip of the rat colon. It is concluded that histamine produced dose-dependent contractions of the guinea-pig colon due to direct activation of H1-histamine receptors. There is no evidence in favour of the existence of H2-histamine receptors in this preparation. The lack of effect of histamine agonists in rat colon strip argues against the existence of histamine receptors in this preparation.

Animals↗
PubMed1987

Dose response relationship of allergen, histamine, and histamine releasers in skin prick test and precision of the skin prick test method.

The aim of the present investigation was to study the dose response relationship of allergen, histamine and histamine releasers in skin prick test (SPT) and the precision of the SPT method. In one experiment timothy allergen, histamine HCl, rabbit anti-human-IgE and compound 48/80 were studied in seven patients. In a second experiment timothy allergen and histamine and dog allergen and histamine were investigated in two groups of 10 patients. Histamine HCl 1 and 10 mg/ml induced weals about 15 and 25 mm2 (4.5 and 5.5 mm in diameter), respectively. The precision as expressed by the coefficient of variation was about 25% for histamine and 40% for allergen for weal areas greater than 10 mm2. Calculations of the regression lines to test the dose response relationships were based on the method of least squares. The best fit was to a log/log model. The slopes of allergen, histamine and histamine releasers were essentially parallel within patients. The median slope of allergen was estimated to about 0.4 based on weal areas and 0.2 based on mean weal diameters. Furthermore, no significant differences were found between the lower and upper parts of the dose response curves of allergen and histamine, although there was a tendency towards steeper slopes at lower concentrations. These results show that histamine concentrations greater than or equal to 1 mg/ml should be used as positive control in SPT and that histamine releasers do not offer advantages over histamine as reference substances in SPT. A common slope for the dose response relationship of allergen and histamine can be used for the estimation of skin sensitivity.

Adolescent↗
PubMedDate not supplied

Effects of histamine and histamine antagonists on hepatic bile flow in the conscious sheep.

The effects of histamine and histamine antagonists on bile flow have been studied using the cholecystectomized conscious sheep. Histamine stimulated bile flow in a dose-dependent manner (D50 = 15.7 micrograms/h per kg). Free water and HCO3-output were increased after intravenous histamine infusion. With histamine at 120 mg/h per kg, there was a 41.0 (s.d. = 4.6)% and 38.7 (s.d. = 4.2)% (n = 6) increase in bile volume and HCO3-output respectively. Bile salt concentration was decreased after intravenous histamine, but net bile salt secretory rate remained unchanged. There was no change observed in the molar ratios of bile salts: phospholipids: cholesterol. Total lipids were decreased from 2.2 (s.d. = 0.3) to 1.60 (s.d. = 0.4) g/dl (n = 6). The corrected lithogenic index did not change significantly. 14C-Erythritol clearance also increased during histamine infusion in a dose-dependent manner but did not correspond to increments in bile flow. The histamine H1-receptor antagonist, diphenhydramine 0.05-1.0 mg/h per kg did not alter histamine stimulated bile flow. The H2-receptor antagonists, cimetidine (0.5-4 mg/h per kg) and ranitidine (0.05-0.5 mg/h per kg) progressively reversed the histamine-induced choleresis. Maximum inhibitory effect was attained at 2.0 and 0.25 mg/h per kg for cimetidine and ranitidine, respectively. At these levels, variation of intravenous infusion of histamine did not result in competitive displacement of the inhibitory response by either cimetidine or ranitidine. Moreover, concomitant infusion of diphenhydramine at 1.0 mg/h per kg potentiated the inhibitory effect of cimetidine or ranitidine on histamine-induced choleresis. Histamine increases the bile salt independent component of hepatic bile flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Functional characteristics of histamine receptor-bearing mononuclear cells. I. Selective production of lymphocyte chemoattractant lymphokines with histamine used as a ligand.

Mitogens and antigens have been the traditional ligands for activating lymphocytes in vitro for the elaboration of lymphokines. Recently, histamine, by interaction with histamine-type 2 receptors on T lymphocytes, has been found to induce the production of one lymphokine, histamine-induced suppressor factor (HSF), that inhibits lymphocyte proliferation and lymphokine production in vitro. Because the biologic effects of HSF appear to be confined to alterations in lymphocyte function, we assessed the ability of soluble products of histamine-stimulated human blood mononuclear cells to affect another lymphocyte function, motility. Utilizing a modified Boyden chamber assay to assess lymphocyte migration, we identified chemoattractant activity for human blood and rat splenic T lymphocytes in histamine-induced mononuclear cell supernatants. No neutrophil or monocyte chemoattractant activity was present. Sephadex G-100 gel filtration of histamine-induced supernatants showed the lymphotactic activity eluted with a 56,000 m.w. This activity was cationic as determined by its elution pattern from a Sephadex QAE anion exchange matrix with a single pl of 9.0 to 9.4 determined by isoelectric focusing in sucrose. Its biologic activity is predominantly chemokinetic in nature, is stable to heating at 56 degrees C for 30 min, but is sensitive to the effects of trypsin and neuraminidase. These physicochemical and functional characteristics establish it as identical to a recently described concanavalin A-induced (Con A) lymphotactic lymphokine (LCF). Mononuclear cells that did not adhere to a histamine affinity matrix were unable to produce LCF when subsequently stimulated with histamine or Con A. Mononuclear cells incubated with histamine and diphenhydramine produced LCF; the addition of cimetidine eliminated LCF production. In fact, supernatants from cells incubated with histamine and cimetidine significantly inhibited lymphocyte migration, a phenomenon explainable by the two regions of lymphocyte migration inhibitory activity that were present in the Sephadex G-100 chromatography of crude histamine-induced supernatants. These data suggest that a subset of lymphocytes defined by the presence of histamine-type 2 receptors is capable of producing LCF while cells that bear histamine-type 1 receptors produce lymphocyte migration inhibitory activity.

Adult↗
PubMed2001

Effect of central and peripheral actions of histamine and its metabolite N-alpha methyl histamine on gastric secretion and acute gastric lesions.

N alpha-methylhistamine (N alpha-MH) is one of unusual metabolite of histamine that was found in Helicobacter pylori-infected stomach and is believed to interact with specific histamine H1, H2 and H3-receptors to stimulate gastric acid secretion and gastrin release from isolated G-cells but the effects of N alpha-MH on gastric mucosal integrity have been little studied. This study was designed; 1) to compare the effect of intraperitoneal (i.p.), intracerebroventricular (i.c.v.) and gastric topical (intragastric i.g.) application of exogenous N alpha-MH with that of standard histamine on gastric secretion in rats equipped with gastric fistula (series A) and 2) to compare the effect of i.c.v. administration of histamine and N alpha-MH with that of peripheral (i.p. and i.g.) application of these amines on gastric lesions induced by 100% ethanol (series B) in rats with or without capsaicin-induced deactivation of sensory nerves. The area of gastric lesions was determined planimetrically, gastric blood flow (GBF) was assessed by H2-gas clearance method and venous blood was collected for determination of plasma gastrin levels by RIA. N alpha-MH and histamine (0.1-10 mg/kg i.p. or i.g.) dose-dependently increased gastric acid output (series A); whereas i.c.v. administration of histamine or N alpha-MH inhibited dose-dependently this secretion; the dose attenuating gastric acid output by 50% (ED50) being 4 and 6 microg/kg i.c.v. Both, N alpha-MH and histamine (2 mg/kg i.p. and i.g.) attenuated significantly the area of gastric lesions induced by 100% ethanol (series B) while producing significant rise in the GBF and plasma immunoreactive gastrin increments. Central application of N alpha-MH and histamine (0.01-5 microg/kg i.c.v.) inhibited ethanol-induced gastric damage whereas higher doses ranging from 10-100 microg/kg of histamine and N alpha-MH were significantly less effective. Capsaicin-induced deactivation of sensory nerves by itself augmented significantly ethanol damage and attenuated significantly the protective and hyperemic effects of histamine and its methylated analog applied i.p. but failed to affect significantly those caused by i.c.v. administration of these amines. We concluded that: 1) central histamine and N alpha-MH inhibits gastric acid secretion and exhibits gastroprotective activity against ethanol in similar manner to that afforded by parenteral and topical histamine and N-alphaMH, 2) central N-alphaMH- and histamine-induced protection involve the enhancement in gastric microcirculation unrelated to neuropeptides released from capsaicin-sensitive afferent nerves, and 3) the major difference between central and peripheral histamine and its methylated analog is the influence on gastric acid secretion which does not appear to play any major role in gastroprotective activity of these agents.

Animals↗
PubMed2002

Molecular modeling and site-specific mutagenesis of the histamine-binding site of the histamine H4 receptor.

The histamine H4 receptor is a novel G-protein-coupled receptor with a unique pharmacological profile. The distribution of H4 mRNA suggests that it may play a role in the regulation of immune function, particularly with respect to allergy and asthma. To define the histamine-binding site of this receptor, molecular modeling and site-directed mutagenesis were used to predict and alter amino acids residing in the histamine-binding pocket. The effects of these alterations on histamine binding and receptor activation were then assessed. Our results indicate that Asp94 (3.32) in transmembrane region (TM) 3 and Glu182 (5.46) in TM5 are critically involved in histamine binding. Asp94 probably serves as a counter-anion to the cationic amino group of histamine, whereas Glu182 (5.46) interacts with the N(tau) nitrogen atom of the histamine imidazole ring via an ion pair. In contrast, Thr178 (5.42) and Ser179 (5.43) in TM5 are not significantly involved in either histamine binding or receptor activation. These results resemble those for the analogous residues in the H1 histamine receptor but contrast with findings regarding the H2 histamine receptor. Our results also demonstrate that Asn147 (4.57) in TM4 and Ser320 (6.52) in TM6 play a role in receptor activation but are not involved in histamine binding. Taken together, these data indicate that although histamine seems to bind to the H4 receptor in a fashion similar to that predicted for the other histamine receptor subtypes, there are also important differences that can probably be exploited for the discovery of novel H4-selective compounds.

Amino Acid Sequence↗
PubMed1999

Cysteinyl leukotrienes mediate histamine hypersensitivity ex vivo by increasing histamine receptor numbers.

BACKGROUND: Hyperresponsiveness to histamine is a key feature of a variety of pathological conditions, including bronchial asthma, food allergy, colitis ulcerosa, and topical allergic disorders. Cells isolated from hyperresponsive individuals do not display exaggerated histamine responses ex vivo and thus the molecular mechanisms underlying histamine responsiveness remain obscure. Importantly, several in vivo observations implicate cysteinyl leukotrienes as possible mediators of increased histamine responses. We decided to investigate whether cysteinyl leukotrienes enhance the cellular reaction to histamine in cell types involved in pathological and immunological histamine hyperresponsiveness, as this might provide an in vitro system for studying histamine responsiveness and could shed light on the underlying molecular mechanisms. MATERIALS AND METHODS: Histamine responsiveness was determined by measuring histamine-induced prostaglandin E(2) production. Scatchard analysis was performed to determine the number of histamine H(1) receptors. Mouse macrophages, primary isolated human peripheral blood monocytes, and human umbilical smooth muscle cells were investigated before and after cysteinyl leukotriene stimulation. RESULTS: In all three cell types tested, cysteinyl leukotrienes instantaneously enhanced histamine-induced prostaglandin E(2) production. This increase in prostaglandin E(2) production coincided with the immediate and transient appearance of additional H(1) receptors on the plasma membrane. CONCLUSIONS: Cysteinyl leukotrienes prime histamine responses by recruiting additional histamine receptors in immunologically relevant cell types in vitro.

Animals↗
PubMed1986

Evidence for rapid histamine turnover and loss of histamine from immature rat mast cells.

Histamine synthetic activity which is high in young mast cells decreases as the cells mature [Beaven et al., J. Pharmac. exp. Ther. 224, 620 (1983)]. In this study we show that a substantial proportion of newly formed histamine in young mast cells leaked to the extracellular environment. The cells acquired the full ability to sequester newly formed histamine once the numbers of intracellular granules and the supply of sulfated mucopolysaccharide material within them had increased. Rat peritoneal mast cells were separated into successive fractions of increasing size and maturity by counter current elutriation. Loss of histamine from fractions of immature cells was demonstrated by a progressive accumulation of histamine in the medium without any decrease in intracellular histamine content. The estimated turnover time of histamine was less than 10 hr. In fractions of more mature cells, the proportion of cellular histamine released into the medium was substantially lower, giving estimated turnover times of 20 hr or longer. Studies with radiolabeled histidine also indicated that little, if any, newly formed histamine was lost from fractions of mature cells. Both release of endogenous histamine and formation of radiolabeled histamine from labeled histidine were inhibited by the histidine decarboxylase inhibitor alpha-fluoromethylhistidine (10 microM). Histamine turnover times were similar in the presence or absence of external histidine, a possible indication that the supply of intracellular histidine was sufficient to maintain normal histamine synthetic activity.

Animals↗
PubMed1981

Histamine suppression of in vivo eosinophil accumulation and histamine release in human allergic reactions.

Although it has been shown that histamine inhibits antigen-induced in vitro histamine release from basophils, it is unclear whether histamine inhibits in vivo mediator release in human allergic reactions. We report effects of exogenous histamine on histamine release and inflammatory cell responses in antigen-challenged skin sites in eight ragweed-sensitive individuals. Four heat-suction blisters in each subject were unroofed, and a collection chamber was appended to each blister base. Chamber A contained 1000 PNU/ml ragweed extract; chamber B contained buffered saline (control fluid); chamber C contained 1000 PNU/ml ragweed and 50 ng (5 x 10(-7) M) of histamine; and chamber D contained histamine alone (50 ng). Comparative analyses of chamber histamine levels in individual subjects showed that (1) histamine levels in chamber A were significantly greater than those in chamber B (p less than 0.01) and that histamine levels in chamber C were not significantly different than those in chamber D (p less than 0.5). Likewise, comparison of eosinophils attaching to membrane filters appended to the chamber bases for 2 hr showed that there were significantly more eosinophils in chamber A than in chamber B (p less than 0.01) and that there was no significant difference in eosinophil numbers on filters appended to chamber C vs chamber D. In three of four subjects studied, addition of exogenous histamine (50 ng/ml) to ragweed before intradermal injection inhibited the ultrastructural mast cell alterations seen within 10 min after injection of ragweed alone. In the one subject in which mast cell alterations were not prevented, exogenous histamine also did not inhibit antigen-induced histamine release or subsequent eosinophil accumulation in the skin chambers.

Eosinophils↗
PubMed1984

Release of histamine by sympathetic nerve stimulation in the guinea pig heart and modulation of adrenergic responses. A physiological role for cardiac histamine?

Histamine has been reported to attenuate adrenergic responses in cardiovascular tissues. In guinea pig atria preloaded with [3H]norepinephrine, histamine diminishes the field stimulation-induced efflux of radioactivity; this effect has been attributed to an inhibition of norepinephrine release from nerve endings. To assess the possible physiological relevance of these findings, we have reinvestigated the effects of histamine on cardiac sympathetic responses and on the release of endogenous norepinephrine in the guinea pig heart isolated with its intact sympathetic innervation. Heart rate, left ventricular contractile force, and perfusion pressure all increased with increasing frequencies of sympathetic nerve stimulation (2-8 Hz). Histamine (3 X 10(-8) to 3 X 10(-7) M) caused dose-dependent attenuation of the responses to sympathetic stimulation. The ability of histamine to modulate nerve stimulation-induced norepinephrine overflow into the coronary effluent was dependent on whether the heart had been preloaded with norepinephrine. Whereas histamine did not cause a significant reduction in nerve stimulation-induced norepinephrine overflow in hearts from untreated animals, histamine significantly reduced stimulation-induced norepinephrine overflow in hearts from guinea pigs that had been pretreated with norepinephrine before sacrifice. Histamine also attenuated the increases in left ventricular contractile force, perfusion pressure, and heart rate, which result from the intracardiac administration of norepinephrine (0.16-microgram bolus injection). In this respect, histamine was as effective as it was in inhibiting the responses elicited by nerve stimulation. Thus, in normal animals, the negative modulatory effect of histamine on adrenergic responses can be attributed largely, if not totally, to a postjunctional mechanism. In contrast, a prejunctional action of histamine may contribute significantly to the negative modulation observed in norepinephrine-preloaded hearts. Since we have observed a large increase in the amount of endogenous histamine present in the coronary effluent after sympathetic stimulation (930 pg during the 30 seconds poststimulation vs. 240 pg during 30 seconds prestimulation), as well as a prolongation of nerve stimulation-induced cardiac responses in the presence of the H2 receptor antagonist tiotidine, we postulate that histamine plays a physiological role as a modulator of sympathetic responses in the heart.

Animals↗
PubMed1991

Controlled clinical trials and cross-sectional studies with plasma histamine measurements and histamine receptor antagonists: solving the problem of preoperative H1- + H2-prophylaxis by asking new questions?

The problem of a preoperative histamine H1- + H2 - prophylaxis was tackled by a group of new studies including randomized controlled clinical trials and cross-sectional studies with plasma histamine measurements and administration of H1- + H2 - antagonists to a control group. The first study demonstrated serial histamine release in the induction of anaesthesia up to 4 times in a single patient. Basal plasma histamine levels in resting subjects fell below 100 pg/ml during the time necessary for preparation of the surgical patient. Hence, spikes of elevated plasma histamine concentrations corresponded to histamine release. Although this histamine release very often was less than 1 ng/ml plasma histamine, it created systemic reactions after atracurium. The cut-off point of 1 ng/ml for such anaphylactoid reactions does no longer exist, also lower plasma levels are of patho-physiological significance. The clinical signs of histamine release in the induction of anaesthesia vary from drug to drug. Sometimes tachycardia and hypertension produce the highest likelihood ratio, sometimes tachy- and bradycardia, but no changes in blood pressure as in the case of atracurium. It is concluded that the reasons why histamine release in anaesthesia and surgery is so much underreported and under-estimated include the present paradigms about plasma histamine levels and the "classical picture" of histamine release. Both are no longer valid and need a re-assessment.

Adolescent↗
PubMed1984

Pharmacological characterization of histamine H2 receptors on clonal cytolytic T lymphocytes. Evidence for histamine-induced desensitization.

Cultured cytolytic T lymphocytes of clonal origin were screened for histamine-stimulated cyclic AMP production. Histamine caused a 2- to 8-fold elevation of cyclic AMP levels in five independent clones. The EC50 for histamine of 1.7 X 10(-5) M and the rank order of potencies of H1 and H2 agonists [impromidine greater than histamine greater than dimaprit greater than 4-methylhistamine greater than 2-methylhistamine greater than 2-(2-aminoethyl)-thiazole] were characteristic of the conventional histamine H2 receptor. H1 and H2 antagonists inhibited histamine-stimulated cyclic AMP elevation with inhibition constants typical for those found on other H2 receptor systems. Prior incubation of cells with histamine resulted in a marked loss in responsiveness to subsequent histamine challenge. We demonstrate that this desensitization is dose and time dependent and results in a change in the efficacy and not the potency of histamine. Although cyclic AMP increases could also be elicited with isoproterenol, prostaglandin E1 or forskolin, desensitization of histamine had no effect on the ability of these agents to stimulate cyclic AMP production. In contrast to the rapid rate of histamine-induced desensitization, recovery of histamine responsiveness could not be detected for several hours.

1-Methyl-3-isobutylxanthine↗
PubMed1999

Histamine induced homologous and heterologous regulation of histamine receptor subtype mRNA expression in cultured endothelial cells.

Histamine has been proposed to play an important role in early inflammatory responses, based on studies documenting the effects of histamine on vasodilation and permeability of microvascular endothelium, as well as histamine-stimulated neutrophil adhesion to endothelial cells. The complex and heterogeneous biological mechanisms of histamine-mediated responses are not yet completely characterized. One of the factors defining inflammatory responses stimulated by histamine might be the distribution and density of receptor subtypes on cell membranes. The aim of this study was to assess whether the regulation of histamine receptor mRNA levels represents a control point in histamine-stimulated processes. Histamine-induced regulation of histamine receptor subtype expression was studied in vitro by semiquantitative RT-PCR analysis of total RNA extracted from stimulated and unstimulated endothelial cells. The time dependency and extent of histamine induced down-regulation varied between the H1 and H2 receptor message. The rapid decrease of H2 receptor mRNA lasted for 24 h. On the other hand, the less-pronounced reduction of H1 mRNA was transient and returned to control values after 12 h of histamine stimulation. The H2 receptor message was mainly down-regulated by activation of the H1 receptor protein. Down-regulation of the H1 receptor message seemed to be a net result of H1 and H2 receptor activation. This is the first report demonstrating a complex pattern of homologous and heterologous regulation of histamine receptor expression. These findings reveal new insight into the potential diversity of the mechanism involved in processing information via stimulation of multiple G-protein-linked pathways.

Cells, Cultured↗
PubMedDate not supplied

Histamine intolerance-like symptoms in healthy volunteers after oral provocation with liquid histamine.

Histamine in food at non-toxic doses has been proposed to be a major cause of food intolerance causing symptoms like diarrhea, hypotension, headache, pruritus and flush ("histamine intolerance"). Histamine-rich foods such as cheese, sausages, sauerkraut, tuna, tomatoes, and alcoholic beverages may contain histamine up to 500 mg/kg. We conducted a randomized, double-blind, placebo-controlled cross-over study in 10 healthy females (age range 22-36 years, mean 29.1 +/- 5.4) who were hospitalized and challenged on two consecutive days with placebo (peppermint tea) or 75 mg of pure histamine (equaling 124 mg histamine dihydrochloride, dissolved in peppermint tea). Objective parameters (heart rate, blood pressure, skin temperature, peak flow) as well as a total clinical symptom score using a standardized protocol were recorded at baseline, 10, 20, 40, 80 minutes, and 24 hours. The subjects received a histamine-free diet also low in allergen 24 hours before hospitalization and over the whole observation period. Blood samples were drawn at baseline, 10, 20, 40, and 80 minutes, and histamine and the histamine-degrading enzyme diamine oxidase (DAO) were determined. After histamine challenge, 5 of 10 subjects showed no reaction. One individual experienced tachycardia, mild hypotension after 20 minutes, sneezing, itching of the nose, and rhinorrhea after 60 minutes. Four subjects experienced delayed symptoms like diarrhea (4x), flatulence (3x), headache (3x), pruritus (2x) and ocular symptoms (1x) starting 3 to 24 hours after provocation. No subject reacted to placebo. No changes were observed in histamine and DAO levels within the first 80 minutes in non-reactors as well as reactors. There was no difference in challenge with histamine versus challenge with placebo. We conclude that 75 mg of pure liquid oral histamine--a dose found in normal meals--can provoke immediate as well as delayed symptoms in 50% of healthy females without a history of food intolerance.

Administration, Oral↗
PubMed1997

Histamine H2 receptor-mediated airway goblet cell secretion and its modulation by histamine-degrading enzymes.

BACKGROUND: Airway goblet cell hypersecretion may contribute to the pathophysiology of asthma. However, it is unknown whether histamine affects goblet cell secretion and, if so, which subtype of histamine receptor is involved and whether endogenous histamine-degrading enzymes modulate these actions. METHODS: We morphometrically assessed goblet cell secretion in the guinea pig trachea stained with alcian blue and periodic acid Schiff stains by measuring the mucus score, which was inversely related to the degree of mucus glycoprotein discharge. RESULTS: Inhalation of histamine caused a dose-dependent decrease in mucus score, an effect that was inhibited by pretreatment with the H2-receptor antagonist cimetidine but not with the H1-receptor antagonist mepyramine or the H3-receptor antagonist thioperamide. Inhaled Dimaprit, a selective H2-receptor agonist, likewise decreased mucus score; whereas stimulation of H1- and H3-receptors with 2-methylhistamine and (R)-alpha-methylhistamine, respectively, had no effect. Pretreatment with the histamine N-methyltransferase inhibitor SKF 91488, but not the diamine oxidase inhibitor aminoguanidine, potentiated the dose-dependent effect of histamine on goblet cell secretion, causing a decrease in the concentration of inhaled histamine required to produce a half-maximal effect from 0.80 +/- 0.12 to 0.48 +/- 0.09 mg/ml (p < 0.01). The histamine methyltransferase activity in the tracheal mucosa was 29 times higher than diamine oxidase activity. CONCLUSION: These findings suggest that histamine stimulates airway goblet cell secretion through H2-receptors and that this effect may be modulated principally by endogenous histamine methyltransferase through a degradation of histamine.

Amine Oxidase (Copper-Containing)↗
PubMedDate not supplied

[Role of histamine as an intermediary in the action of estradiol on the rat uterus: inhibition of the hormonal induction of enzymes using histamine antagonists].

The administration of methiamide, a blocker of histamine H2-receptors, to rats was shown to prevent the induction of hexokinase (HK) and glucose-6-phosphate dehydrogenase (G-6PD) caused by both histamine and estradiol. An inhibitory effect of methiamide remained stable up to 16 h after histamine and estradiol administration. Diphenhydramine, a blocker of histamine H1-receptors, produces a short-term inhibitory effect on the HK and G-6PD activity stimulated by histamine and estradiol. The short-term nature of the diphenhydramine effect may be attributed to a low affinity to histamine H2-receptors and histamine fast dissociation. It may be concluded that some of the estradiol effects, particularly the HK and G-6PD induction in the uterus are histamine-mediated, apparently by means of H2-receptors. The administration of histamine to rats increases the uterus mass causing its inundation, and H1- and H2-blockers prevent this effect of histamine. However, the above histamine antagonists do not inhibit uterus inundation caused by estradiol. A conclusion is made that estradiol stimulates the uterus inundation not only by means of histamine but also by some other means.

Animals↗
PubMed1980

Sensory responses of human skin to synthetic histamine analogues and histamine.

The potential for itch production in human skin of the synthetic analogues of histamine, 2-methyl histamine (an H1-receptor agonist) and 4-methyl histamine and dimaprit (H2-receptor agonists) has been studied in vivo and compared with histamine. Itch thresholds for 2-methyl histamine were consistently much higher than for histamine (P < 0.001). The H1-receptor antagonist chlorpheniramine raised the itch thresholds to 2-methyl histamine and histamine significantly (P < 0.001). Pruritus was not obtained with either 4-methyl histamine or dimaprit. No evidence of synergism between 2-methyl histamine and either 4-methyl histamine or dimaprit was found. The results suggest that histamine-induced pruritus is mediated in part through the H1-receptor and in part via an additional (but probably non-H2) mechanism.

Adult↗