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PubMed1976

Stimulation of adenylate cyclase of guinea pig gastric mucosa by histamine, sodium fluoride and 5'-guanylylimidodiphosphate and inhibition by histamine H1- and H2-receptor antagonists in vitro.

There are experimental data indicating that cyclic AMP is involved in the regulation of gastric acid secretion in various mammalian species. In a broken cell preparation of guinea pig gastric mucosa the effects of some stimulants of gastric acid secretion on the activity of adenylate cyclase were studied. The basal adenylate cyclase activity was 483 +/- 43 pmoles cyclic AMP/mg protein x 10 min. The activity could be stimulated by histamine maximally 5-fold, by sodium fluoride (NaF) maximally 20-fold and by 5-guanylylimidodiphosphate (GMP-PNP) maximally 10-fold. Neither pentagastrin nor carbachol were able to stimulate the adenylate cyclase. Stimulants of adrenergic alpha- or beta-receptors (phenylephrine, isoproterenol) were also ineffective. The activation of the adenylate cyclase by histamine was inhibited by the histamine H1-receptor antagonists diphenhydramine and mepyramine as well as by the histamine H2-receptor antagonist metiamide. On the other hand, the stimulatory action of NaF OR GMP-PNP could be antagonized only by high concentrations of dipenhydramine or mepyramine while metiamide showed no antagonizing effect in this respect. Thus this preparation can be used as a tool to determine the activity and specificity of histamine H2-receptor antagonists.

Adenylyl Cyclase Inhibitors↗
PubMed1985

Histamine receptor activation by unsaturated (allyl and propargyl) homologs of histamine.

The spectrum of agonist activity for three new homologs of histamine (cis- and trans-imidazolylallylamine and imidazolylpropargylamine) was evaluated in the isolated guinea pig ileum and right atrium. The homologs were about three log units less potent than histamine in stimulating contractions of the longitudinal muscles of the ileum, but they were histamine-like, pharmacologically, because they were sensitive to blockade by pyrilamine and resistant to blockade by atropine. In the right atrium, these weak agonists were partially sensitive to blockade by cimetidine. The agonist activity of the cis-isomer in particular was completely blocked by a combination of cimetidine and propranolol, but resistant to reserpine treatment (neuronal catecholamine depletion). Therefore, these homologs of histamine have the ability to stimulate H1- and H2-histamine receptors and beta-adrenoreceptors in vitro.

Adrenergic Fibers↗
PubMed1990

Histamine release from human peripheral blood leukocytes analyzed by histamine radioimmunoassay.

Histamine release from human peripheral blood leukocytes, after in vitro challenge with allergen extracts, is usually measured by fluorometry. In the present study we compared the results of the automated fluorometric histamine assay (Siraganian) with those of the Immunotech histamine radioimmunoassay. Histamine release dose-response curves obtained after histamine measurement by both methods were superimposable.

Histamine↗
PubMed1984

Surface histamine receptors in rat peritoneal mast cells. Separation of receptor-bearing cells via binding to a histamine-protein conjugate, Cell-ect.

The Seragen Cell-ect Total Histamine KitTM was used to separate histamine receptor-bearing rat peritoneal mast cells from cells lacking these receptors. It was found that approximately 75% of the peritoneal mast cell population carried cell surface histamine receptors. The results further suggest that the mast cell histamine receptors present are mainly of an H1-type, as judged by the capacity of a specific H1-antagonist to reduce the histamine receptor-dependent cell adhesion. Moreover, an H1-agonist is less efficient in this respect and an H2-antagonist does not affect the cell adhesion at all. A possible functional role for these receptors, however, remains to be clarified.

Animals↗
PubMed1992

Modulation of IgE-mediated histamine release from human leukocytes by a new class of histamine H2-agonists.

A new class of phenyl (pyridylalcyl) guanidines, acting as potent histamine H2-agonists, inhibits IgE-mediated human basophil histamine release in a nanomolar range. IC30-level of three substitutes of this group (arpromidine, BUA-75, and FRA-19) were found to be 0.02, 0.015 and 0.008 microM. The inhibition appeared with a fast onset (plateau after 10 min. preincubation) and claimed its maximum (60 +/- 2.9%, 63 +/- 1.8%, and 61 +/- 3.1%, n = 7) with 10 microM of the compounds. H2-mediated inhibition was totally blocked by 10 microM famotidine, a potent histamine H2-antagonist. The amount of anti-IgE or antigen for the initiation of the immunological release influenced the strength of inhibition of H2-agonist FRA-19 (p less than 0.05). Combined preincubation of FRA-19 with zardaverine, a cAMP-specific phosphodiesterase III/IV inhibitor, produced a synergistical inhibitory effect of leukocyte histamine release, which might explained by their different sites of action on intracellular cAMP levels. The capability of histamine to inhibit its own release is mediated by H2-receptors exclusively. New, potent H2-receptor stimulating compounds with positive inotropic effects possess additional potent anti-allergic properties.

Basophils↗
PubMed1981

The effect of captopril on plasma histamine and histamine release in vitro.

Plasma histamine and the release of histamine from blood in vitro has been determined in patients being treated for hypertension or heart failure with captopril. This drug does not alter plasma histamine levels in either group of patients or release histamine from human basophils, rat peritoneal mast cells or guinea pig lung slices upon challenge in vitro. We conclude that histamine release does not contribute to the cardiovascular or side effects of captopril.

Adult↗
PubMed1989

Correlation between urinary levels of histamine metabolites in 24-hour urine and morning urine samples of man: influence of histamine-rich food.

In this study, we have determined and correlated the excretion of the 2 most important histamine metabolites, N tau-methylhistamine and N tau-methylimidazoleacetic acid, in 24-hour urine and morning urine samples of 14 normal healthy persons. We found no significant difference between morning urine and 24-hour urine samples, provided that the subjects were on a histamine-poor diet for at least 24 hours. We also studied the influence of the consumption of histamine-rich foodstuffs on the reliability of these parameters. The morning urinary N tau-methylhistamine excretion is less affected by histamine-rich food-stuffs and therefore proposed to be the most reliable parameter for endogeneous histamine release.

Adult↗
PubMed1992

Intracellular histamine and liver regeneration: high affinity binding of histamine to chromatin, low affinity binding to matrix, and depletion of a nuclear storage pool following partial hepatectomy.

We have demonstrated in rat hepatocytes that 3H-histamine binds specifically to novel low (microM) and high (nM) affinity sites, designated "HIC" to denote their intracellular location. Low affinity HIC sites are associated with microsomes, while both low and high affinity HIC sites are associated with the nucleus. A growth-regulatory action of intracellular histamine at HIC, independent of the rise in cytosolic calcium, has been demonstrated in mitogen-stimulated lymphocytes. We now report that the high affinity HIC sites in liver cell nuclei are associated exclusively with chromatin, while only low affinity sites are found in the residual material containing the nuclear matrix. Moreover, hepatocyte nuclei contain histamine (approximately 1 ng/mg protein), unaffected by incubation for up to 18 hours with the histidine decarboxylase inhibitor, alpha-FMH, suggesting a slow rate of turnover typical of a storage pool. A decrease in nuclear histamine parallels a rise in DNA synthesis in the first 24 hours after partial hepatectomy. Our findings support a role for a nuclear pool of pre-formed histamine in the mediation of liver regeneration.

Animals↗
PubMed1988

Optimization of histamine radio enzyme assay with purified histamine-N-methyltransferase.

The radio enzyme assay for histamine based on the transmethylation with purified histamine-N-methyltransferase and utilizing [3H-methyl]-S-adenosylmethionine as the methyl donor has been optimized to measure low histamine concentrations, for example in plasma. The pH-optimum for the assay is pH 8.3 in Tris-glycine buffer at 20 degrees C. An incubation time of 90 min is necessary using an enzyme concentration of 5.8 micrograms/ml. EDTA and dithiothreitol were included in the assay to keep the histamine-N-methyltransferase active as agents that oxidize -SH groups were found to be inhibitory to the reaction. The present assay is sensitive to about 0.5 nmol/l of histamine in a sample volume of 50 microliter (about 3 pg/sample).

Animals↗
PubMed1989

Comparison between number of basophils, blood histamine, and histamine release in cancer and noncancer patients.

In cancer patients with primary tumor with or without metastasis or metastasis alone, by comparison with healthy subjects and noncancer patients, the decrease in blood histamine levels is due to a decrease in total basophil number. These basophils have a normal content of histamine (1 to 2 pg per basophil) and are able to release histamine. The percentage of anti IgE-induced histamine release is not significantly different than in noncancer patients. The scarcity of basophils in cancer patients is not due to a leukopenia. Blood histamine levels and total basophil number are normal in patients after successful excision of their primary tumor without metastasis.

Adult↗
PubMed1992

Possible role of histamine in pathogenesis of autoimmune diseases: implications for immunotherapy with histamine-2 receptor antagonists.

The immunosuppressive chemical drugs cyclosporine A (CsA) and methotrexate (Mx) have recently been shown to be of benefit in several different diseases of autoimmune origin. Cellular immune responses may play a major role in autoimmunity as autoreactive T lymphocytes appear to recognize autoantigens and major histocompatibility complex (MHC) class II restriction molecules presented by non-immune, aberrant cells, subsequently leading to damage on healthy tissues. Psoriasis is suggested to be an autoimmune disease and in severe, uncontrollable psoriasis CsA and Mx are of value in reducing disease activity. Histamine is suggested to be involved in the pathogenesis of psoriasis and the histamine-2 receptor antagonist ranitidine has been shown to be of value to reduce severe psoriatic disease. The finding that CsA and Mx efficiently reduce histamine formation and release raises the possibility, that histamine is one of the molecules involved in pathogenesis of autoimmune diseases. T cell mediated regulation and suppression of autoreactive T cells seem to be ineffective in controlling the enhanced immune reaction in patients where the discrimination between self and non-self is changed. A consequence of this may be induction of interferon-gamma (IFN-g) production and release by cytotoxic T cells, subsequently leading to expression of MHC II molecules on non-immune tissues. As immunotherapy may be of value in some autoimmune diseases the use of histamine-2 receptor antagonists should be evaluated in patients where conventional therapy is ineffective to reduce disease activity.

Autoimmune Diseases↗
PubMed2000

Effects of drugs acting as histamine releasers or histamine receptor blockers on an experimental anxiety model in mice.

Experimental anxiety in mice was evaluated using a light/dark test at 60 min after injection of various histaminergics. Thioperamide, a histamine H(3) receptor inhibitor (5-20 mg/kg, intraperitoneal [IP]), Compound 48/80, a mast cell degranulator (0.1-10 microg/2 microl, intracerebroventricularly [ICV]), mepyramine, a histamine H(1) receptor antagonist (0.1-10 microg/2 microl, ICV) or cimetidine, a histamine H(2) receptor antagonist (0.1-10 microg/2 microl, ICV) alone did not affect the locomotive activity, the time spent in the light zone, and number of shuttle crossings in the light/dark test. However, the time spent in the light zone and the number of shuttle crossings significantly decreased only when cimetidine (0.1-10 microg/2 microl, ICV) was co-treated with either thioperamide (10 mg/10 ml/kg, IP) or Compound 48/80 (1.0 microg/2 microl, ICV). The decrease in these behavioral parameters suggests induced experimental anxiety in mice. The experimental anxiety was antagonized by mepyramine (10 microg/2 microl, ICV). These results suggest that not only neuronal histamine release induced by thioperamide but also non-neuronal (mast cells) histamine release induced by Compound 48/80 play an important role in inducing experimental anxiety via post-synaptic H(1) and H(2) receptors. In addition, it is likely that the anxiety may be mediated by the stimulation of H(1) receptors, while H(2) receptors may inhibit the anxiety produced by the activation of H(1) receptors.

Animals↗
PubMed1987

Effect of cetirizine, a new histamine H1 antagonist, on airway dynamics and responsiveness to inhaled histamine in mild asthma.

Cetirizine, a major human metabolite of hydroxyzine, preserves the histamine H1-antagonist activity of the parent compound but poorly penetrates the blood-brain barrier, thus minimizing sedative and anticholinergic effects. In 10 young (mean age 27.7 years) subjects with mild asthma (FEV1 greater than 70% predicted), we evaluated the bronchodilator and protective efficacy of 5, 10, and 20 mg of cetirizine against bronchospasm induced by histamine inhalation (0.03 to 20 mg/ml) in comparison with placebo and hydroxyzine, 25 mg, using a random, double-blind crossover design. The provocative concentration of histamine causing a 20% decline in FEV1 for all 10 subjects from the postdiluent control value was more than fourfold greater after each active drug than after placebo. Cetirizine, 5 to 20 mg, provided significantly greater protection against histamine-induced bronchospasm than hydroxyzine (p less than 0.001); moreover, a dose-dependent protective effect was noted with cetirizine. Significant bronchodilation was also found: at 60 minutes, FEV1 increased significantly after all active antihistamines compared to placebo and after 20 mg of cetirizine compared to hydroxyzine (p less than 0.05). FEV1 increased significantly at 120 minutes after hydroxyzine and after cetirizine in both the 20 and 10 mg doses compared to placebo (p less than 0.05). We conclude that in subjects with mild asthma, orally administered cetirizine provides significant dose-dependent protection against histamine-induced bronchoconstriction, which in the doses studied is superior to that produced by the parent compound, hydroxyzine. In addition, cetirizine in 5 to 20 mg doses causes acute bronchodilation. These results suggest a possible role of cetirizine in asthma therapy.

Administration, Inhalation↗
PubMed1985

[Evolution of plasma histamine after midazolam in patients at risk of histamine liberation].

Changes in plasma histamine levels 2 min (t1) and 10 min (t2) after the intravenous injection of 0.2 mg X kg-1 midazolam were measured in 10 subjects at risk of releasing histamine (group I) and compared with those of 15 other subjects free from any risk of releasing histamine (group II). There was mean increases in plasma histamine levels of 0.78 ng X ml-1 between t0 and t1 (p less than 0.01), and of 0.41 ng X ml-1 between t0 and t2 (p less than 0.01) in group I; they only rose by 0.18 ng X ml-1 between t0 and t2 (p less than 0.01) in group II. The only statistically significant variation between the two groups was that at t1 (p less than 0.03): plasma histamine levels rose higher at the second minute in those cases at risk. This was a rather small increase, within physiological limits, and without any clinical or haemodynamic manifestation.

Adult↗
PubMed1988

Ionized calcium influences gastrin stimulated histamine release and acid secretion, but not histamine stimulated acid output in the totally isolated vascularly perfused rat stomach.

When changing from bovine serum albumin to dextran T70 as colloid without adjusting the total calcium concentration in the vascular perfusate of the totally isolated vascularly perfused rat stomach, we noticed a drastic fall in gastrin-stimulated acid secretion. In the present study the effect of the two colloids on ionized calcium in the vascular perfusate as well as the effect on acid secretion and vascular histamine release were studied. There was no difference in gastrin-stimulated acid secretion or vascular histamine release between the two colloids after adjusting the total calcium concentrations so that ionized calcium was similar. Whereas baseline acid secretion showed no marked dependency of ionized calcium within the range tested (0.73-1.54 mmol l-1, gastrin-stimulated acid secretion was highly dependent on ionized calcium being reduced at the higher concentration of Ca2+. Histamine stimulated acid secretion, on the other hand, was virtually unaffected by the concentration of ionized calcium in the same range. Like gastrin-stimulated acid secretion, gastrin-stimulated histamine release was inhibited at higher Ca2+ concentrations. Thus, elevated Ca2+ concentrations seemed to reduce gastrin-stimulated acid secretion by inhibiting vascular histamine release.

Animals↗
PubMed1998

Histamine-stimulated cytokine secretion from human conjunctival epithelial cells: inhibition by the histamine H1 antagonist emedastine.

The present studies demonstrate that histamine induces the secretion of IL-6, IL-8 and GM-CSF from human conjunctival epithelial cells in a dose- and time-dependent manner. The histamine antagonists emedastine (H1), ranitidine (H2) and thioperamide (H3) were evaluated for their ability to inhibit secretion of these cytokines. Emedastine potently inhibited histamine-induced IL-6, IL-8 and GM-CSF secretion with mean IC50 values of 2.23, 3.42 and 1.50 nM, respectively. Ranitidine and thioperamide failed to inhibit cytokine secretion over a wide dose range. These data suggest that mast cell derived histamine may stimulate inflammatory cytokine production in allergic conjunctivitis via activation of epithelial cell H1 receptors. The histamine H1 antagonist emedastine potently inhibits this response.

Benzimidazoles↗
PubMedDate not supplied

Increased hyaluronan flux in canine paw lymph is induced by histamine and the histamine-releasing agent compound 48/80.

The present experiments investigated hyaluronan (HYA) flux from skin of pentobarbital anesthetized mongrel dogs when transcapillary fluid flux was increased by local intraarterial injection of histamine (50 micrograms) or Compound 48/80 (C48/80) (100 micrograms) inducing mast cell degranulation. A prenodal lymphatic draining the hindpaw was cannulated and the paw flexed passively at 50 times/min. Grand mean (n = 18) of control lymph flow and HYA concentration was 16 +/- (SD) 14 microliters/min and 8.8 +/- 2.3 micrograms/ml, respectively. Lymph flow increased 11- and 15-fold within 10 min after histamine and C48/80 injection, respectively, and returned to control values after 3 h for histamine while it did not return fully in the C48/80 group. HYA concentration decreased by 30 and 40% during the first hour after histamine and C48/80, respectively, while HYA flux increased 11-15 times control. Control experiments (saline vehicle) showed an unexpected and gradual increase in HYA concentration during the 8-hour experimental period, regardless of unchanged lymph flow. This increase became statistically significant at the end of the experimental period, suggesting either an increased synthesis or increased rate of release of bound HYA from the paw. The present data show that HYA is loosely bound and easily mobilized from the interstitial matrix and that histamine and C48/80 cause a release of bound HYA from the interstitium. An increase in HYA concentration towards the end of the 8-hour experimental period most likely represents an increased synthesis of HYA.

Animals↗
PubMed1985

Histamine receptors on leukocytes: the binding of histamine serum albumin conjugates is non-specific.

It is commonly held that certain leukocyte sub-populations adhere selectively to histamine-serum albumin conjugates. A large number of soluble histamine, ethylamine and dimethylaminopropylamine conjugates were synthesised and labelled with fluorescein isothiocyanate (FITC). Although a number of conjugates bound to mononuclear cells and granulocytes our data showed this binding to be non-specific. The binding of histamine conjugates to leukocytes was not inhibited by preincubation of cells with free histamine at concentrations of up to 10(-1) M nor was it pH sensitive. In addition, conjugates of ethylamine and dimethylaminopropylamine showed a similar binding pattern to that of histamine conjugates. We suggest that the observed binding may be due to modifications to the net charge of the carrier protein molecule.

Carrier Proteins↗