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At least 199 records · Page 11Linked to original sources
PubMed1993

Histamine N-methyltransferase modulates histamine- and antigen-induced bronchoconstriction in guinea pigs in vivo.

To examine whether histamine N-methyltransferase (HMT; EC 2.1.1.8) modulates the effects of allergic reaction in vivo, we studied the effects of aerosolized SKF 91488, a specific HMT inhibitor, on the responses to aerosolized histamine in unsensitized guinea pigs and to ovalbumin (OA) antigen inhalation in guinea pigs sensitized to OA. Airway responsiveness was assessed by determining provocation concentrations of histamine and OA aerosols that increased pulmonary resistance to twice the baseline values. SKF 94188 shifted, in a dose-dependent fashion, the dose-response curves to histamine and OA antigen to lower concentrations, and it significantly decreased provocation concentrations of both histamine and OA antigen (p < 0.01). In contrast of SKF 91488, aerosolized aminoguanidine, a specific inhibitor of diamine oxidase (10(-2) M, 90 breaths), did not alter the provocation concentration of histamine (p > 0.20). SKF 91488 (10(-2) M, 90 breaths) caused no significant changes in response to acetylcholine (p > 0.30). HMT activities were observed in the entire airways of the trachea, main bronchi, segmental bronchi and bronchioles, and parenchymal tissues. These findings suggest that HMT modulates the effects of exogenous histamine and endogenously released histamine by antigen challenge on bronchoconstrictor responses in guinea pigs in vivo.

Aerosols↗
PubMed1981

Characterization of neuronal and vascular histamine receptors mediating the salivary and vasodilator responses to histamine of the dog submandibular gland.

The submandibular gland in situ was perfused with blood through the glandular artery at constant pressure in anesthetized dogs, and all drugs were administered intra-arterially. During infusion of metiamide, histamine and 2-(2-pyridyl)ethylamine (PEA) produced salivary and vasodilator responses consisting of an early and a late component. The dose-response curves for respective components of the salivary and vasodilator responses to PEA were parallel with the corresponding curves for histamine and in producing these responses PEA was about 40 times less potent than histamine on a molar basis. During infusion of mepyramine, histamine and dimaprit produced only the early vasodilator response. The dose-vasodilator response curves to histamine and dimaprit were parallel, and dimaprit was about 750 times less potent than histamine on a molar basis. The present results support the conclusion obtained in a previous study that neuronal histamine receptors mediating the whole salivary and the late vasodilator response are exclusively of the H1-type and vascular histamine receptors mediating the early vasodilator response consist of both H1-and H2-type although the former is predominant.

Animals↗
PubMed1989

Histamine content and histamine H1 receptor in experimentally-induced nasal hypersensitivity.

Quantitative evaluations of histamine and histamine H1 receptor were carried out in nasal mucosa of toluene diisocyanate (TDI) sensitized guinea-pigs at specific points in time during a pre-determined sensitization period. Histamine content is significantly increased at 1 week and definitely elevated after 2 weeks of sensitization. This increase was maintained throughout the sensitization period. It decreased to normal by four weeks post-sensitization. Also the relatively low histamine content immediately after TDI challenge indicated that a certain amount of histamine was released by TDI challenge. On the other hand, the density and affinity of the histamine H1 receptor was not found to be altered during TDI sensitization. These results suggest that enhanced histamine has a role in the development of nasal allergy, whereas the relevance of quantitative-alteration of the H1 receptor to histamine hypersensitivity observed in nasal allergy has not been demonstrated.

Animals↗
PubMedDate not supplied

Methoxyphenamine inhibits histamine-induced bronchoconstriction in anaesthetized guinea-pigs and histamine-induced contractions of guinea-pig ileum in vitro.

Measurements were made of the effects of methoxyphenamine hydrochloride on histamine-, acetylcholine- and U46619-induced bronchoconstriction in pentobarbitone-anaesthetized guinea-pigs, and on histamine- and acetylcholine-induced contractions of guinea-pig ileum in vitro. Methoxyphenamine (20 mg/kg, i.v.) did not affect bronchoconstriction induced by acetylcholine or the thromboxane A2-mimetic U46619. However, it produced a parallel rightward shift [2.94-(1.79, 4.41) fold, 95% confidence limits in parentheses] of the curve relating bronchoconstrictor responses to log-dose of histamine at a total dose of 13 mg/kg, i.v., which was not significantly different from the shift [3.30-(1.93, 5.56) fold] produced by 3 micrograms/kg, i.v., of the histamine antagonist mepyramine maleate. Histamine-induced contractions of the isolated guinea-pig ileum were antagonized by methoxyphenamine (10(-5) to 10(-3) M). The histamine log-concentration-response curve was shifted to the right in a parallel manner by methoxyphenamine (10(-5) to 10(-4) M), without depression of maximum responses. However, at higher concentrations, maximum responses were reduced. The slope of the Schild plot was significantly different from -1. The degree of the rightward shift of the concentration-response curves to histamine, produced by 10(-5) M of methoxyphenamine [3.90-(2.83, 4.97) fold], was not significantly different from that produced by 3 x 10(-9) M of mepyramine [4.60-(2.86, 6.52) fold]. Methoxyphenamine, at concentrations of 10(-5) to 3 x 10(-4) M, had no significant effect on responses of guinea-pig ilea to acetylcholine (10(-9) to 10(-5) M). These results indicate that methoxyphenamine antagonizes the effects of histamine both in vivo and in vitro. In vitro studies indicate a noncompetitive antagonism.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1989

Stimulation of gastric alkaline secretion by histamine in rats: possible involvement of histamine H2-receptors and endogenous prostaglandins.

The mechanism of stimulatory action of histamine on gastric alkaline secretion was investigated in anesthetized rats. Intravenous infusion of histamine (2-8 mg/kg/hr) dose-dependently stimulated acid secretion and in the presence of omeprazole (60 mg/kg), an H+/K+-adenosine triphosphatase inhibitor, produced an increase of gastric but not duodenal alkaline secretion; the degree of gastric alkalinization was also dependent on the dose of histamine, reaching the maximal values of approximately 1.0 microEq/10 min. Cimetidine (100 mg/kg s.c.) significantly inhibited both acid and alkaline secretory responses caused by histamine, whereas indomethacin (5 mg/kg s.c.) significantly prevented the increased alkaline secretion caused by histamine as well as mucosal acidification (100 mM HCl for 10 min). Tripelennamine (10 mg/kg s.c.) had no effect on either acid or alkaline secretion. Histamine (8 mg/kg/hr) reduced the arterial blood pressure (25.3%) and increased the mucosal vascular permeability in the stomach as determined by Evans blue (160%), but these vascular responses were significantly prevented only by tripelennamine, excluding the possible contribution of the vascular effects to the increased gastric alkaline secretion. These results suggest that histamine may stimulate gastric alkaline secretion as well as acid secretion, and the mechanism of histamine-induced alkaline secretion may involve both endogenous prostaglandins and stimulation of H2-receptors.

Animals↗
PubMed1981

Evidence for a role of endogenous histamine in central cardiovascular regulation: inhibition of histamine-N-methyltransferase by SKF 91488.

Studies were undertaken to determine whether changes in endogenous brain histamine levels would occur concomitant with centrally mediated cardiovascular responses. All experiments were performed on conscious rats since previous findings by others have indicated anesthesia alters cardiovascular responses. Rats were injected intracerebroventricularly (i.c.v.) with SKF 91488 (10-100 micrograms), a potent inhibitor of histamine-N-methyltransferase, while blood pressure and heart rate were recorded. In all animals, there was a dose-related increase in mean arterial blood pressure and a fall in mean heart rate after this treatment. These responses were very similar to the cardiovascular effects observed after i.c.v. injections of exogenous histamine (0.1-5.0 micrograms). Within 5 min after i.c.v. injection of SKF 91488, there was a statistically significant increase in hypothalamic histamine levels; within 15 min, histamine levels were significantly elevated in the cerebral cortex, hypothalamus and the remainder of the brain. In other experiments, cardiovascular responses after i.c.v. injection of histamine were potentiated by prior treatment with SKF 91488. It is concluded that brain histamine is involved in central cardiovascular regulation and that the hypothalamus may be a site of action. These results also imply a neurotransmitter role for histamine in the mammalian brain.

Animals↗
PubMed1981

The histamine-like effects of tolazoline and clonidine:: evidence against direct activity at histamine receptors.

Both tolazoline and clonidine produce agonist effects sensitive to histamine H2-receptor antagonism in whole animals and a variety of isolated tissues. In guinea-pig right atria, tolazoline concentration-response curves were shifted to the right and progressively depressed by cimetidine. Clonidine produced a submaximal histamine-like tachycardia which was converted by cimetidine to a depression of sinus rate. Neither tolazoline nor clonidine stimulated histamine H2-receptors in rabbit right atria. Instead, these agents were very weak inhibitors of histamine with a pA2 for tolazoline of 3.3 and for clonidine of 3.7. No appreciable histamine H1-receptor activity was evident for either drug in experiments with guinea-pig ileum. The weak histamine H2-receptor affinity is inconsistent, from a quantitative point of view, with the hypothesis that the agonist activity results from direct stimulation of histamine receptors, but all data re compatible with previous evidence which suggests that these drugs release endogenous histamine.

Animals↗
PubMed1994

A novel fluorescein-histamine reagent to quantitate histamine receptor expression on leucocytes.

The expression of histamine receptors on the surface of rat lymph node cells was studied using a reagent made by directly coupling fluorescein isothiocyanate (FITC) to histamine. This approach contrasts with the use of previous reagents, made by coupling histamine and fluorescein separately to a protein carrier, which bind non-specifically to cells and cause staining unrelated to histamine receptor expression. The new reagent was used, in combination with a panel of monoclonal antibodies, for the dual staining of rat lymph node cells for two-colour flow cytometric analysis to investigate the distribution of histamine receptors on different leucocyte subsets. The majority of cells were stained by the FITC-histamine reagent and these constituted two distinct populations, those with the properties of small lymphocytes and a second population which included macrophages. Inhibition studies with the drugs mepyramine and cimetidine, which are antagonists of H1 and H2 receptors, respectively, showed that most lymphocytes possess H1 receptors while the macrophages have H2 receptors. It seems that macrophages have a higher number of histamine receptors than the majority of lymphocytes, but that they are of lower affinity.

Animals↗
PubMed1977

A comparison of the effects of bradykinin, 5-hydroxytryptamine and histamine on the hepatic arterial and portal venous vascular beds of the dog: histamine H1 and H2-receptor populations.

1 The hepatic arterial and hepatic portal venous vascular beds of anaesthetized dogs were separately perfused in different experiments.2 From measurements of perfusion pressures and blood flows in the two series of experiments, hepatic arterial vascular resistance (HAVR) and hepatic portal venous vascular resistance (HPVR) respectively were calculated.3 Bradykinin, 5-hydroxytryptamine (5-HT) and histamine were injected intra-arterially and intra-portally and dose-response curves constructed from these data.4 Bradykinin injected intra-arterially caused dose-dependent hepatic arterial vasodilatation, and with an ED(50) of 2.66 x 10(-13) mol was more potent than any other vasodilator agent yet examined on this vascular bed.5 Bradykinin injected intraportally at doses up to 10 times those which were maximal on the arterial circuit did not alter the calculated HPVR.6 5-HT injected intra-arterially caused weak and variable rises in HAVR, indicating vasoconstriction. The maximum rise in HAVR was much less than that attained with noradrenaline in the same preparations.7 5-HT injected intraportally caused dose-dependent rises in HPVR indicating portal constriction at doses above 15-100 mug: in some experiments small doses of 5-HT resulted in reductions in calculated HPVR.8 Histamine has previously been shown to cause hepatic arterial vasodilatation: by intraportal injection, it caused dose-dependent rises in HPVR.9 In order to examine the receptors responsible for the effects of histamine, dose-response curves were constructed before and after mepyramine and metiamide.10 On the hepatic arterial vascular bed, metiamide did not antagonize the vasodilator effects of intra-arterial histamine, but these effects were antagonized by mepyramine.11 Similarly on the hepatic portal bed, the rises in HPVR due to histamine were antagonized by mepyramine but not by metiamide.12 The effects of histamine on both the hepatic arterial and portal venous vascular beds of the dog are therefore mediated predominantly by histamine H(1)-receptors.

Animals↗
PubMed1989

[Histamine distribution in the uterine structures of ovariectomized rats administered estradiol, histamine antagonists and an inhibitor of prostaglandin synthesis].

In the experiments performed on ovariectomized rats, using luminescent-histochemical method for revealing histamine after Cross, Ewen and Rost, it has been demonstrated that estradiol facilitates increasing histamine content in the uterine structures, as well as its redistribution--histamine content increases in the glandular and tegmental epithelia, in stromal cells, smooth myocytes and it decreases in macrophages. These manifestations of estradiol action are absent after cymetidin and indometacin, but not tavegil administration. The first two inhibit the morphological effect of estradiol in the uterus, indometacin making it in a greater degree. It is supposed that estradiol action, concerning provision of the uterine structures with histamine, takes place together with prostaglandins participation and at hormonal activation of H2-receptors. Taking into account the literature data on stimulating influence of estradiol on macrophagal phagocytosis and secretion, a conclusion is made that decreasing content of histamine in macrophages at estrogenization results from histamine release by these cells; macrophages are potential sources of histamine in the uterus.

Animals↗
PubMed1981

Effect of histamine and histamine antagonists on the glycogen content of Tetrahymena.

The glycogen content of Tetrahymena pyriformis was analysed by a cytophotometric method. Histamine and histamine antagonists were found to influence the glycogen content. It increases after acute histamine treatment, while it decreases after 4 days incubation with histamine. The H2 receptor antagonist methiamide was more effective than histamine, while the H1 receptor antagonist phenindamine had no effect on the glycogen content. The effect reflects the similarity or dissimilarity of the chemical structure of the antagonists and of histamine. Subdivision of the cytophotometric results indicated that all of the protozoa react to histamine or to its antagonists, but all agents increased the number of glycogen-rich Tetrahymena.

Animals↗
PubMed1986

Histamine in endocrine cells in the stomach. A survey of several species using a panel of histamine antibodies.

Antibodies to histamine were used to examine the localization of the amine in cells of the stomach and upper small intestine of a great variety of species, including cartilaginous and bony fish, amphibia, reptiles (lizard), birds (chicken) and a large number of mammals. In all species gastric histamine was localized in endocrine cells (invariably found in the epithelium) and mast cells (usually with an extra-epithelial localization). The endocrine cells were identified as such by immunostaining with antibodies to chromogranin A and the mast cells were identified by toluidine blue staining. Histamine-immunoreactive endocrine cells were found almost exclusively in the acid-producing part of the stomach; only rarely were such cells observed in the pyloric gland area. They were fairly numerous in the gastric mucosa of the two subclasses of fish as well as in the amphibia and reptile species studied. Here, the majority of the histamine-immunoreactive endocrine cells seemed to have contact with the gastric lumen (open type cells) and were located in the surface epithelium (certain fish only) or together with mucous neck cells at the bottom of the pits. In the chicken, histamine-immunoreactive endocrine cells were numerous and located peripherally in the deep compound glands. They were without contact with the lumen (closed type) and had long basal extensions ("paracrine" appearance), running close to the base of the oxyntic-peptic cells. In mammals, the number of histamine-immunoreactive endocrine cells in the stomach varied greatly. They were particularly numerous in the rat and notably few in the dog, monkey and man. In all mammals, the histamine-immunoreactive endocrine cells were of the closed type and located basally in the oxyntic glands. They often had a "paracrine" appearance with long basal processes. Histamine-storing mast cells, finally, were few in both subclasses of fish as well as in the amphibian species and in the lizard. They were fairly numerous in chicken proventriculus (beneath the surface epithelium), few in the oxyntic mucosa of mouse, rat and hamster, moderate in number in hedgehog, guinea-pig, rabbit, pig and monkey, and numerous in cat, dog and man.(ABSTRACT TRUNCATED AT 400 WORDS)

APUD Cells↗
PubMed1986

Rat jejunal mucosal response to histamine and anti-histamines in vitro. Comparison with antigen-induced changes during intestinal anaphylaxis.

We previously showed that rats sensitized to egg albumin (EA) respond in vivo intraluminal antigen-challenge with decreased net absorption of water and electrolytes and depletion of mucosal histamine. However, administration of anti-histamines did not prevent the transport abnormalities. The present in vitro studies examined the effect of histamine to alter net ion transport and the ability of diphenhydramine (DPH) and cimetidine (CIM) to block the responses to both histamine and antigen. Control rat jejunum was mounted in Ussing chambers and histamine was added to the serosal side either in the absence or presence of DPH or CIM. In control tissues histamine caused a transient increase in short-circuit current (Isc) in a dose-dependent manner between 10(-5) and 10(-4) M which was blocked by 10(-5) M DPH but was unaffected by CIM in concentrations up to 10(-4) M. There was no response to EA. Jejunum from sensitized rats exposed to EA demonstrated a biphasic Isc response: a rapid transient rise followed by a somewhat less elevated but sustained component. In tissues pre-treated with DPH the initial peak was unaffected but the sustained component was reduced. Our results indicate that H1-receptors mediated the effects of histamine in rat jejunal mucosa but that during intestinal anaphylaxis histamine is responsible for only a portion of the antigen-induced transport abnormalities. Our data also suggest that IgE-mediated reactions in the intestine may involve an interaction between mast cell mediators and enteric nerves.

Animals↗
PubMed1987

Histamine as a ligand in blood plasma. Part 7. Malate, malonate, maleate and tartrate as adjuvants of zinc to favour histamine tissue diffusion through mixed-ligand coordination. In vitro tests on lymphocyte proliferation.

Investigations based on computer simulated distributions of histamine in blood plasma were recently devoted to the assessment of the roles of cysteine, aspartic and glutamic acids as possible adjuvants of zinc to favour histamine tissue diffusion through mixed-ligand coordination. Since all tissues contain at least one of the two enzymes required for the catabolism of histamine, any increase of its tissue diffusion is expected to result in an acceleration of its degradation, which may be of interest for the treatment of anaphylactic disorders. As an extension of these studies, the present paper first reports (i) an experimental investigation of the tendency of four dicarboxylic acids, namely malate, malonate, tartrate and maleate, to mixed-ligand coordination with zinc and histamine, (ii) computer-based potential effects to be expected from the association of these agents to zinc with respect to histamine tissue diffusion. Cell culture studies were then used to test simulation expectations. Two series of experiments involving successively human lymphocytes and a lymphoblastoid cell line (8866) have been carried out, which led to the following conclusions: (i) the hypothesis formerly put forward that cysteine could favour histamine tissue diffusion through mixed-ligand coordination with zinc has been validated on the two cell models, (ii) the formerly established suppressive role of histamine versus lymphocyte proliferation has clearly been confirmed, (iii) moreover, this suppressive effect has been shown to occur correlatively to histamine uptake by these cells, (iv) the four dicarboxylic acids, more especially tartric acid, proved effective as catalysts of the two above processes. Possible biomedical applications of these results are discussed.

Cell Line↗
PubMed1992

Oestradiol enhances in vitro the histamine release induced by embryonic histamine-releasing factor (EHRF) from uterine mast cells.

The relationship between maternal hormones and factors secreted by the implanting embryo is still controversial. We have analysed the in-vitro effect of oestradiol and human embryo-derived histamine-releasing factor (EHRF) on histamine release from rat uterine mast cells. Rat uterine mast cells which were preincubated with oestradiol and then challenged with human EHRF gave histamine release values two- to threefold higher than those without preincubation. The enhancement observed was time- and temperature-dependent. A similar enhancement was obtained with human sensitized basophils but not with rat peritoneal mast cells. Oestradiol, used as a direct challenge, did not induce any histamine release from either rat uterine or peritoneal mast cells, or from human sensitized basophils. Oestradiol preincubation also enhanced the histamine release induced by anti-IgE but did not enhance the histamine release induced by substance P or compound 48/80, two secretagogues that are not mediated by IgE. Moreover, uterine fragments derived from rats at various oestrus phases, with different amounts of endogenous oestrogen, were challenged in vitro with EHRF. The release of histamine by mast cells was higher at the proestrus and preimplantation phases than at dioestrus. All these findings suggest that the interaction of oestradiol with rat uterine mast cells was capable of enhancing in vitro the histamine releasing effect of EHRF.

Animals↗
PubMed1983

Effects of histamine and the histamine antagonists mepyramine and cimetidine on human coronary arteries in vitro.

The effects of histamine have been studied on human isolated coronary artery preparations taken from hearts ranging in age from 9 to 73 years. Histamine in large concentrations (100 microM) contracted arteries which were without tone or spontaneous activity and sometimes induced rhythmic contractile activity. If spontaneous rhythmic activity was present it was enhanced by histamine. The contractile effects of histamine were inhibited by mepyramine but not by cimetidine. Arteries which were contracted by depolarization responded with relaxation to histamine concentrations lower than those required to evoke a contraction; arteries from younger hearts were more sensitive than those from older hearts. Mepyramine potentiated the maximal relaxant effect of histamine in arteries from hearts of all ages but cimetidine had very little effect. In the presence of mepyramine, cimetidine antagonized the relaxant effect of histamine, shifting the concentration-effect curve to the right. It is concluded that human coronary arteries contain both H1- and H2-type receptors, the H1-receptors mediating contraction. The relaxant effects of histamine can only be inhibited by a combination of both H1- and H2-receptor antagonists.

Adolescent↗
PubMed2000

Effects of castration and testosterone replacement on peritoneal histamine concentration and lung histamine concentration in pubertal male rats.

Mast cells, which are the main source of histamine, are significantly affected by sex steroids. The present study was undertaken to determine the effects of bilateral castration and testosterone replacement on peritoneal histamine concentration and lung histamine concentration in pubertal male rats (Wistar strain). Three groups of animals were used in this study: (1) untreated castrated animals, (2) castrated animals subjected to androgen replacement by injection of propionate of testosterone, and (3) intact males as a control group. Castration alone produced a dramatic reduction in peritoneal histamine concentration. In addition, androgen replacement was effective in restoring the histamine concentration to the normal value detected in the control males (P<0.05, Kruskal-Wallis test). On the other hand, there was no significant variation in the lung histamine concentration between control males, untreated castrated males and castrated males that received androgen replacement (P<0.05, Kruskal-Wallis test). These results demonstrate for the first time that castration markedly reduces the peritoneum histamine concentration in pubertal male rats, and testosterone replacement prevents the decrease. Further, these procedures do not affect lung histamine concentration, demonstrating that mast cells from different tissues may respond differently to the same biological factors.

Animals↗
PubMed2001

Flow-through chemiluminescence sensor using immobilized histamine oxidase from Arthrobacter crystallopoietes KAIT-B-007 and peroxidase for selective determination of histamine.

A flow sensor with immobilized oxidases is proposed for the determination of histamine in fish meat. Chemiluminometric measurement of histamine was based on the luminol reaction with hydrogen peroxide produced by immobilized histamine oxidase (EC 1.4.3.-.) and peroxidase (EC 1.11.1.7.) within a flow cell. Histamine oxidase was found in cells of Arthrobacter crystallopoietes KAIT-B-007 isolated from soil. The oxidase and peroxidase were coimmobilized covalently on tresylated hydrophilic vinyl polymer beads and packed into transparent PTFE; the tubing was used as the flow cell. One assay for histamine was done at intervals of 2 min without carryover. The calibration curve for histamine was linear from 0.1 microM to 50 microM. The response was reproducible within 1.25% of the relative standard deviation for 115-replicate injections of 50 microM histamine. The sensor system was applied to the determination of histamine in fish meat extracts.

Amine Oxidase (Copper-Containing)↗