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PubMed1984

Gastric mucosal histamine, histamine formation capacity (HFC) and plasma gastrin after cysteamine administration.

Cysteamine administration is followed by stomach and duodenal ulcers in rats. We aimed to establish a time relationship between changes in gastric mucosal histamine, histamine formation capacity (HFC) and plasma gastrin after cysteamine administration. Up to 4 h after cysteamine s.c., no ulcers were found. Plasma gastrin rose after cysteamine and was higher than in controls 2h after injection. Mucosal histamine fell after 4h; no other significant changes were found in mucosal histamine and HFC. A direct correlation was found between plasma gastrin and HFC in both controls and after cysteamine. It is suggested that the changes indicate that cysteamine releases gastrin, which increases HFC and thus histamine. The fall in histamine seems to indicate utilization of histamine in acid production.

Animals↗
PubMed1978

Blood histamine level and histamine content in the lung tissue in immediate immunological reactions in human and experimental animals.

The blood histamine level was determined in 66 patients with bronchial asthma and 25 guinea-pigs in whom the asthma attacks were induced by histamine or ovoalbumin inhalation after previous immunization of the animals. At the same time, histamine content of the lung tissue of the guinea-pigs was determined. It was found that in both humans and animals the level of blood histamine during immediate allergic reactions rises significantly. The extent of this rise depends on intensity of the reaction and time of determination. In asymptomatic period the blood histamine level did not differ from that of the control groups. Histamine concentration in the lung tissue of many of the animals increased during asthma attack but not in all cases was this increase correlated to the rise in blood histamine level. The reasons for these changes are discussed.

Animals↗
PubMed1993

Mast cells and their committed precursors are not required for interleukin-3-induced histamine synthesis in murine bone marrow: characteristics of histamine-producing cells.

In the present study we investigate the nature of the murine bone marrow cell subset responsible for the marked increase in histamine synthesis induced by interleukin-3 (IL-3). Because mast cells, and eventually their committed precursors, represent a potential source of histamine in this context, we examined their possible participation in this biologic activity with particular attention. We provide evidence that neither of these populations respond to IL-3 in terms of histamine synthesis and that other differentiated end cells or stromal components of the bone marrow are also not involved in this phenomenon. Starting from these findings, we further characterized the immature hematopoietic compartment responsible for IL-3-induced histamine synthesis using fluorescence-activated cell sorter (FACS) sorting based on rhodamine retention or wheat germ agglutinin (WGA) affinity. These procedures have allowed us to ascribe the following features to histamine-producing cells: (1) They belong to a low-density, progenitor-enriched bone marrow subset containing cells of relatively important size and internal structure. (2) The highest histamine levels are generated by the rhodamine-bright fraction of this population, while the most primitive rhodamine-dull cells do not express this biologic activity. (3) Histamine-producing cells do not copurify with colony-forming units in spleen day 7 and day 12 in WGA-bright fractions. (4) Their enrichment is associated with increased frequencies of cells forming colonies in methylcellulose (CFU-C), suggesting the involvement of several progenitors with partially limited differentiation potential in this biologic activity.

Animals↗
PubMed1987

Effect of histamine and histamine receptor antagonists on rat mesenteric microcirculation.

Histamine release adjacent to mesenteric arterioles under conditions of ischemia causes vasodilation and increases regional blood flow. This is presumably a protective mechanism which may be blocked by the use of H1 and H2 antagonists. Mesenteric arterioles of 29 rats were observed with intravital microscopy. Diameter and erythrocyte velocity were measured and arteriolar flow was calculated. Histamine was topically applied to the vessels under view in sequentially increasing concentrations (10(-7) to 10(-4) M). Following systemic injection of an H1 or H2 receptor antagonist or ibuprofen, the application of 10(-4) M histamine was repeated. Topical histamine caused vasodilation (122% of control; P less than 0.05) at 10(-4) M with a corresponding increase in erythrocyte velocity and calculated flow (118 and 177% of control, respectively; P less than 0.05 for each). The vasodilatory effects of histamine were blocked by systemic injection of histamine receptor antagonists (H1 + H2 greater than H1 greater than H2), while ibuprofen had no significant effect. In situations in which the gut is at risk for ischemia, the use of H1 and/or H2 receptor antagonists may seriously compromise the mesenteric microcirculation.

Animals↗
PubMed1994

A new model for the agonistic binding site on the histamine H2-receptor: the catalytic triad in serine proteases as a model for the binding site of histamine H2-receptor agonists.

The historical model for the agonistic binding site on the histamine H2-receptor is based on a postulated activation mechanism: it has been suggested that the histamine monocation binds to the histamine H2-receptor via the formation of three hydrogen bonds. The cationic ammonium group in the side chain and the -NH- group in the tau-position of the imidazole act as proton donors, whereas the =N- atom in the pi-position of the imidazole acts as a proton acceptor. Participation of the ammonium group in H-bonding with a presumed negative charge on the receptor leads to a decrease in positive charge, which is thought to induce a tautomeric change in the imidazole ring system from N tau-H to N pi-H. A consequence of this tautomeric shift is the donation of a proton from the receptor to the agonist on one side, while on the other side a proton is donated from the agonist to the receptor. The propose tautomeric shift has been suggested to trigger the H2-stimulating effect. However, this model for the constitution of the agonistic binding site and the accessory activation mechanism cannot explain the weak histamine H2-activity of beta-histine and the activity of several other recently synthesized H2-agonists. Based on a thorough literature study and with the aid of molecular electrostatic potentials (MEPs) we demonstrate that the sulphur atom present in histamine H2-agonists as dimaprit and 2-amino-5-(2-aminoethyl)thiazole does not function as a proton acceptor, which implicitly means that a tautomeric shift is not a prerequisite for H2-stimulation. As a consequence, the model for the agonistic binding site is adjusted, resulting in a strong resemblance to the nature and orientation of the amino acids constituting the catalytic triad in serine proteases. Within this concept, the N pi-H tautomer of histamine is the biologically active form, in contrast with the existing model in which the N tau-H tautomer is the active form.

Animals↗
PubMed2002

Roles of histamine in regulation of arousal and cognition: functional neuroimaging of histamine H1 receptors in human brain.

Brain histamine is involved in a wide range of physiological functions such as regulation of the sleep-wake cycle, arousal, cognition, and memory mainly through interactions with histamine H1 receptors (H1Rs). Neurons producing histamine, histaminergic neurons, are exclusively located in the posterior hypothalamus and transmit histamine to almost all regions of the brain. Histamine H1 antagonists, or antihistamines, often prescribed for treatment of allergic disorders, sometimes induce sleepiness and cognitive deficits. It is understood that the mechanism of such CNS side effects is that antihistamine blocks H1Rs in the brain. The purpose of the present study was to compare the CNS side effects of different antihistamines. Subjective sleepiness was measured using the Stanford Sleepiness Scale (SSS) and psychomotor performance was examined by a tachistoscope testing system in healthy, young, Japanese volunteers (16 males, 20-28 yrs.) before and after oral administration of antihistamines such as fexofenadine (FEX) and cetirizine (CET). Additionally, H1R occupancy by antihistamines was examined by PET with 11C-doxepin in 8 volunteers. The results of SSS and psychomotor tests demonstrated that FEX tended to be less sedative than CET though the difference was not statistically significant. PET measurements revealed that no H1Rs in the cerebral cortex were occupied by FEX while about 30% of H1Rs were occupied by CET. In summary, it was confirmed that histamine and H1Rs are involved in maintaining arousal and cognition in humans, and that the severity of clinical symptoms is correlated to the amount of antihistamine that penetrated into the brain.

Adult↗
PubMed1980

Effect of histamine and histamine antagonists on portal blood pressure in patients with hepatosplenic schistosomiasis.

1 Histamine injection via the cannulated portal vein significantly raised the portal pressure in normal volunteers. This elevation was reversed by an H1-receptor blocker but not an H2-receptor blocker. When an H1-receptor blocker was injected first followed by histamine, no significant change in portal pressure was obtained. On the other hand, an H2-receptor blocker failed to antagonize the effect of histamine. 2 Histamine injection induced a non-significant increase in the portal pressure in patients with schistosomal portal hypertension, but when an H1-receptor blocker was injected a significant drop in the portal pressure was obtained. No similar effect was found after an H2-receptor blocker injection. 3 Angiographic study showed that histamine induced intrahepatic portal vasoconstriction in the normal controls. A similar change was obtained in the schistosomal group, particularly on the periportal neovascular formation. 4 In the light of the present study, it is suggested that histamine may contribute in part to the physiopathologic changes that lead to portal hypertension in hepatosplenic schistosomiasis. H1-receptor antagonists may have a role in the treatment of portal hypertension, particularly in bleeding varices.

Adult↗
PubMed1980

Oxatomide: in vivo assessment of antagonistic activity, and effects on histamine release and enzymatic histamine degradation in skin.

The antagonistic activity of oxatomide, and its effects on evoked histamine release and histamine-N-methyl transferase activity in skin, have been studied. Oxatomide antagonizes H1 activity in a dose-dependent but non-competitive manner. It also shows some atropine-like activity. Oxatomide did not cause detectable inhibition of antigen-stimulated histamine release from skin slices of sensitized guinea-pigs although the possibility that oxatomide may cause weak inhibition could not be excluded. In the presence of low concentrations of histamine, oxatomide suppressed human skin histamine-N-methyl transferase, but in the presence of higher substrate concentrations it enhanced activity of this enzyme. These observations, which were limited by the poor solubility of oxatomide in aqueous media, should encourage further in vivo studies of oxatomide's histamine-suppressing properties in the human subjects.

Acetylcholine↗
PubMed1990

Effect of stobadine and histamine H1 and H2 blockers on histamine-induced contraction of guinea pig airways in vitro.

Histamine, a nonselective histamine receptor agonist, activates simultaneously both H1 and H2 receptors in the guinea pig trachea and lung strip. The resulting contraction is due to the prevalence of H1 receptors, because they are blocked by the selective H1 antagonist diphenhydramine. The H2 receptor antagonists cimetidine and ranitidine increased the sensitivity of both tissues to histamine by affecting primarily the amplitude of contractions induced by high histamine concentrations. Since the lung strips were more sensitized by ranitidine and low concentrations of the other studied antagonists (diphenhydramine, dithiadene, stobadine) than the tracheal smooth muscle, it is inferred that the density of H2 receptors is higher in peripheral than central airways. From all the studied histamine receptor antagonists only dithiadene was able to unmask the relaxation induced by H2 receptor activation indicative of its highest H1 selectivity. In the light of the concentration-dependent antihistaminic effect of stobadine, i.e. potentiation in low and inhibition in high concentrations, stobadine is suggested to belong to antihistaminics with no histamine receptor subtype selectivity.

Animals↗
PubMed1991

Histamine and histamine type-2 receptor antagonists in psoriasis. Mechanisms and speculations.

The findings that the immunosuppressant cyclosporine A (CsA) improves psoriasis raise the possibility that cellular immune processes may play a major role in the pathogenesis of this disease. It is broadly agreed that histamine released by mast cells is one of the molecules involved in the pathogenesis. This is supported by the findings that CsA and methotrexate (Mxt) reduce formation and release of histamine. However, the well known side-effects of CsA and Mxt may argue potential use of other agents acting on formation and action of histamine. Such agents may be the histamine-2 receptor antagonists, previously reported to have a clinical effect on psoriasis. But randomised short-term studies have disclosed that these drugs have no beneficial or even an aggravating effect on the disease. This article reports on recent findings of improvement in psoriasis using high doses of the histamine-2 receptor antagonist ranitidine in long-term studies. Also presented are a hypothetical action of histamine in development of psoriasis and a rationale for ranitidine as a potential agent in the therapy of psoriasis.

Cyclosporine↗
PubMed1980

The role of histamine H-receptors in the anaphylactic histamine release from human basophilic leukocytes.

The effect of two recently synthetized selective histamine H2-receptor agonists on anaphylactic histamine release from human basophilic leukocytes was investigated. It was found that both agonists tested, partially inhibited histamine release induced either by antigen or by human anti-IgE. Cimetidine, the histamine H2-receptor antagonist, generally antagonized this effect. It is concluded that anaphylactic basophil histamine release can be modulated by stimulation of histamine H2-receptors.

Anaphylaxis↗
PubMed1979

Effects of histamine receptor antagonists on histamine-induced responses in human skin.

The effects of intradermally administered histamine H1- and H2-receptor antagonists on the cutaneous responses--redness, weal, flare and itch--induced by intradermal injection of histamine were studied in man. Weal and redness were studied after blockade of the axon reflex by local infiltration with lidocaine. All responses were significantly inhibited by the H1-receptor antagonist mepyramine. The H2-antagonists cimetidine and metiamide reduced flare and itch significantly but not to the same extenet as mepyramine and not in a clearly dose-related manner. The size of weal and redness was not significantly reduced by cimetidine. No further reduction of flare, itch or weal was obtained by adding metiamide or cimetidine to mepyramine. After blockade of the axon reflex with lidocaine the histamine-induced weals turned white at the centre. This blanching was more prominent when histamine was injected in combination with cimetidine. Substituting mepyramine for cimetidine resulted in small weals with an intense red colour. It is concluded that, apart from being engaged in the direct vasodilatory response to histamine, H2-receptors do not seem to be involved in the other cutaneous responses to histamine studied.

Adult↗
PubMedDate not supplied

Lack of the specific influence of histamine and histamine H1, H2 and H3 receptor ligands on the serotonin uptake and release in rat blood platelets.

This work was designed to investigate the influence of histamine, and H1 receptor agonist 2-(2-thiazolyl)ethylamine, H2 receptor agonist dimaprit and H3 receptor agonist R-(-)-alpha-methylhistamine on the serotonin uptake and release in rat blood platelets. Histamine and R-(-)-alpha-methylhistamine (up to 1 mmol/l), 2-(2-thiazolyl)ethylamine (up to 10 mumol/l) and dimaprit (up to 1 mumol/l) failed to affect the serotonin uptake. The concentration-dependent inhibitory effects of higher concentrations of 2-(2-thiazolyl)ethylamine and dimaprit (up to 1 mmol/l) were not diminished by the H1 receptor antagonist dimetindene and the H2 receptor antagonist ranitidine (1 and 100 mumol/l each), respectively. Histamine, 2-(2-thiazolyl)ethylamine, dimaprit and R-(-)-alpha-methylhistamine (up to 10 mumol/l) did not change the serotonin release from rat blood platelets. Our results demonstrate that histamine and histamine H1, H2 and H3 receptor agonists do not affect in a specific manner the serotonin uptake and release in rat blood platelets.

Animals↗
PubMed1988

Long-term depletion of histamine in guinea-pigs by administration of alpha-fluoromethylhistidine, a specific inhibitor of histidine decarboxylase; effect on the sensitivity of histamine receptors.

The effect of intraperitoneal administration of alpha-fluoromethylhistidine (alpha-FMH), a specific inhibitor of histidine decarboxylase, at a dose of 100 mg/kg twice a day for 6 weeks on the sensitivity of histamine receptors in the guinea-pigs was examined. The histamine contents in the ileum, heart and brain after the treatment decreased to about 54%, 83% and 9-62% (depending on the region), respectively, of those of controls. However, there were no significant difference in the histamine-induced contraction of the ileum and atrium, the maximal binding (Bmax) and the dissociation constant (Kd) of [3H]-mepyramine binding to membrane fractions of the ileum and brain (except the cortex) and the increase of cyclic AMP formation induced by histamine in membranes of the heart and brain (except the cortex) between alpha-FMH-treated- and untreated animals. These results suggest that long-term histamine depletion dose not significantly affect the sensitivity of histamine receptors of guinea-pig except in the brain cortex.

Adenylyl Cyclases↗
PubMed1987

Histamine response in developing chick oesophagus. A pharmacological analysis of the response to histamine in the oesophagus of developing chick.

Developmental changes in response to histamine were investigated in the oesophagus isolated from the chick between 15 days of incubation and 15 days after hatching. The contraction could be already caused by histamine (20 microM) in the chick oesophagus from 15 days of incubation. The pD2 values for histamine and acetylcholine did not change during the period between 17 days of incubation and 5 days after hatching. The response to histamine (20 microM) was extremely resistant to tetrodotoxin (0.78 microM), procaine (0.2 mM) and atropine (1 microM) during the period between 17 days of incubation and 20 days of incubation. The tetrodotoxin-resistant response was replaced by a tetrodotoxin-sensitive response after hatching. On the other hand, the neuronal response induced by transmural electrical stimulation (20 Hz) or dimethylphenylpiperazinium (20 microM) was uniformly sensitive to tetrodotoxin throughout the periods. Mepyramine (2 microM), but not metiamide (20 microM), inhibited the histamine-induced responses in every age tested. These results suggest that the myogenic receptivity of histamine transiently increases during the terminal period of embryonic development and declines after hatching.

Acetylcholine↗
PubMed2003

Analysis of histamine and modeling of ligand-receptor interactions in the histamine H(1) receptor for Magic Angle Spinning NMR studies.

OBJECTIVE AND DESIGN: Investigation of the principles of ligand-receptor interaction in histamine receptors can help to provide a solid foundation for structure-based drug design. Stable isotope labelling of the ligand 'Histamine' has been performed and 1D (13)C CP MAS and 2D Radio Frequency Dipolar Recoupling (RFDR) spectra for the ligand are presented. Hyperfine signals were well spread and did not suffer from any sizable line broadening. The production of H(1) receptor for Magic Angle Spinning NMR studies is currently in progress. TREATMENT: An agonist binding domain is proposed using homology modeling, database searches and mutagenesis data for the H(1) receptor. METHODS: Homology modeling, Database searches for Expressed sequence Tag (ESTs), Magic Angle Spinning Nuclear Magnetic Resonance analysis of the ligand histamine. RESULTS: The three-dimensional receptor model and mutagenesis studies suggest that the amine of the agonist histamine may form an ion pair with the TM III Asp, whereas the imidazole ring of histamine may associate with TM V Asp and Thr. CONCLUSIONS: Homology modeling studies confirms the absence of TM VIII in the H(1) receptor. According to the model the histamine in particular interacts with the transmembrane (TM) regions of the H(1) receptor structure, in particular TM helix III and V. This is in line with recent mutagenesis studies. Database search methods for ESTs have been used for electronic prediction of tissue distribution of H(1) receptor expression. The results indicate that the H(1) expression is highest in heart and skeletal muscle, which may be of importance for drug targeting.

Biophysical Phenomena↗
PubMed1976

Automated histamine analysis for in vitro allergy testing. I. A method utilizing allergen-induced histamine release from whole blood.

A sensitive, automated, histamine assay system has been developed and applied for in vitro allergy testing. Nine common pollen and environmental allergens were used at three log dilutions for in vivo studies utilizing small volumes of blood (15-20 ml). The clinical evaluation was correlated with the results of the histamine release. two different procedures were utilized. The first is the commonly used histamine release from washed leukocytes. There was excellent correlation between the clinical evaluation and the results of histamine release from washed leukocytes in 17 different individuals. The second and simpler method utilized whole heparinized blood which might better reflect the immunologic reaction which occurs in vivo. Aliquots of blood and allergen were incubated for 1 hr at 37 degrees C and each supernatant was then analyzed for histamine release. There was excellent correlation between the two tests in 29 patients tested by both the whole blood and washed leukocyte methods. There was also good correlation between the clinical evaluation of the patients amd the intro tests. The precision, accuracy, and sensitivity of the automated histamine assay make feasible its routine application in the clinical study of allergic patients.

Allergens↗
PubMed2006

Histamine augments beta2-adrenoceptor-induced cyclic AMP accumulation in human prostate cancer cells DU-145 independently of known histamine receptors.

Androgen-independent prostate cancer cells DU-145 express a number of G protein-coupled receptors, including histamine H1 receptors. There is evidence for the presence of beta-adrenoceptors in the human prostate, and in this work we set out to characterise the expression of beta-adrenoceptors by DU-145 cells, their linking to cyclic AMP (cAMP) formation and the possible modulation by histamine H1 receptors of beta-adrenoceptor function. Saturation [3H]-dihydroalprenolol binding indicated that DU-145 cells express moderate levels of beta-adrenoceptors (22.7+/-2.5 fmol/mg protein), which belong to the beta2-subtype as assessed by inhibition by the antagonists ICI-118,551 and CGP-20712A. Inhibition of [3H]-dihydroalprenolol binding by agonists (noradrenaline, adrenaline and isoproterenol) showed the presence of both high-(53-59%) and low-affinity binding sites. beta-Adrenoceptor stimulation with isoproterenol resulted in robust [3H]-cAMP accumulation (10-30-fold of basal, EC50 142 nM; pEC50 6.85+/-0.05). While not having effect of its own on basal [3H]-cAMP accumulation, histamine significantly augmented the beta2-adrenoceptor-induced response (overall effect 152+/-6% of isoproterenol alone) with EC50 1.35 microM (pEC50 5.87+/-0.06). This effect was independent of extracellular Ca2+, insensitive to antagonists/agonists at H1, H2 or H3/H4 receptors and mimicked by drugs containing an imidazole ring in their chemical structure and by imidazole itself. Taken together, our results show that in DU-145 cells histamine augments beta2-adrenoceptor-induced cAMP independently of the activation of known histamine receptors. The effect may involve other mechanisms such as allosteric modulation of beta2-adrenoceptors by the imidazole moiety of histamine.

Cell Line, Tumor↗