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At least 19 recordsLinked to original sources
PubMed1979

The effect of histamine-1 and histamine-2 antagonists on airway responses to histamine in the rhesus monkey.

This study used rhesus monkeys with consistent respiratory responses to aerosolized histamine. Two systems of histamine challenge were evolved to study the effects of histamine antagonists on the histamine-induced respiratory response. One system consisted of administering increasing subreactive concentrations of histamine until an airway response (H) occurred. This threshold histamine dose was repeated (H'). The pulmonary function changes occurring with the H' challenge were less intense than those with H. M, a histamine-2 receptor antagonist, when given before the H' dose was associated with a potentiated H' response compared with the threshold H response. This provides evidence for histamine-2 receptor sites in rhesus monkey airways. A second system used duplicate histamine challenges with a known reactive dose of histamine. In this system, the pulmonary function changes occurring with the repeated challenge (H') were greater than with the first reactive challenge dose (H). This H' response was inhibited partially with diphenhydramine, a histamine-1 receptor antagonist. These two systems of histamine challenge provide an experimental model for evaluating pharmacologic alteration of histamine-induced respiratory responses. There is evidence for the existence of histamine-1 and histamine-2 receptor sites in the airways of the rhesus monkey.

Animals↗
PubMed1978

Histamine enhances anaphylactic histamine release from bovine lung and leukocytes via histamine H2-receptor.

Chopped lung and isolated leukocytes of calves sensitized to horse plasma release histamine when incubated with the antigen. Low concentrations (10(-9) and 10(-8) M) of exogenous histamine enhanced both spontaneous and antigen-induced histamine release. The enhancement of antigen-induced histamine release was inhibited by metiamide but not by mepyramine, whereas the enhancement of spontaneous histamine release was not significantly affected by either histamine antagonist. At higher concentrations of exogenous histamine (10(-6) to 10(-4) M), uptake and metabolism significantly interfered with the method. These results indicate the existence in bovine lung and leukocyte of a positive feedback mechanism which regulates histamine release via an H2-receptor. This is in direct contrast to the reported situation in the human leukocyte, and suggests that histamine fulfils an important role in the intrinsic control of allergic reactions in cattle.

Anaphylaxis↗
PubMed1977

Histamine-releasing effect of a corticotrophin derivative. I. Histamine-releasing effect of a nonadecapeptide in comparison with that of other histamine liberators.

The histamine-liberating properties of a synthetic polypeptide (an a synthetic polypeptide (an alkylprolyl derivative of beta1-19-corticotrophin) were investigated under a variety of experimental conditions. It was found to be more potent in this respect than Compound 48/80, Melittin and Triton X-100. The degree of cell destruction observed in conjunction with the release of histamine induced by C 44 680-Ba suggests that the mode of action of the substance more closely resembles that of Compound 48/80 than that of Triton.

Adrenocorticotropic Hormone↗
PubMed1979

Differentiation of the roles of histamine H1- and H2-receptors in the mediation of the effects of histamine in the isolated working heart of the guinea-pig.

1 Differentiation of the roles of histamine H1- and H2-receptors in the mediation of the effects of histamine on the isolated working heart of the guinea-pig was achieved through the use of histamine and selective histamine receptor agonists and antagonists. 2 Histamine over the dose range 10(-9) mol to 10(-6) mol produced dose-related increases in sinus rate, left intraventricular pressure (LVP)max, LVdP/dtmax, coronary flow, aortic flow, total cardiac output and external pressure-volume work. 3 Dimaprit, a selective histamine H2-receptor agonist, produced very similar responses to histamine. 4 2-Pyridylethylamine, a selective histamine H1-receptor agonist, had little effect on cardiac function unless large doses were administered. Such doses produced increases in all measured parameters. 5 Cimetidine, a selective histamine H2-receptor antagonist, antagonized the effects of histamine and dimaprit and some but not all effects of 2-pyridylethylamine. In the presence of cimetidine a decrease in all parameters with the exception of sinus rate was observed with both histamine and 2-pyridylethylamine. 6 The selective histamine H1-receptor antagonist, mepyramine, had little effect on responses to all three agonists. However, the depressant effects observed with histamine and 2-pyridylethylamine in the presence of cimetidine were antagonized by mepyramine. 7 The results indicate the important role of the histamine H2-receptor in the mediation of the gross cardiac effects of histamine and also indicate that histamine H1-receptors can mediate cardiac depression.

Animals↗
PubMed1975

Histamine receptors in adipose tissue: involvement of cyclic adenosine monophosphate and the H2-receptor in the lipolytic response to histamine in isolated canine fat cells.

The effects of histamine on lipolysis and associated changes in adenosine 3',5'-monophosphate (cyclic AMP) levels were examined in the isolated canine fat cell. Histamine, like norepinephrine, caused a dose-dependent increase in free fatty acid (FFA) and glycerol levels. The lipolytic response to histamine was preceded by a rise in the levels of cyclic AMP and was greatly potentiated by the addition of theophylline. In isolated canine fat cells, histamine (2 muM) caused a 7-fold increase in FFA levels. This effect was inhibited more than 50% in the presence of insulin (0.4 mmu/ml) or prostaglandin E1 (2.8 muM). In similar experiments, cyclic AMP Levels were increased 11-fold by histamine (2 muM) in the presence of 1 mM theophylline. Burimamide (0.1 mM), a histamine H2-receptor antagonist, reduced the effect of histamine (2 muM) on FFA levels as well as the effect on cyclic AMP levels greater than 95% but did not inhibit the lipolytic response to norepinephrine (2 muM). Propranolol (0.01 mM), a beta adrenergic antagonist, reduced the lipolytic response to norepinephrine by 97% but did not inhibit the effects of histamine on FFA or cyclic AMP levels. Tripelennamine and 1,5-diphenyl-3-dimethylaminopyrrolidine, histamine H1-receptor antagonists, inhibited neither the lipolytic response to histamine nor the effect on cyclic AMP levels. It was concluded that histamine induces lipolysis in canine fat cells by a mechanism involving cyclic AMP and the histamine H2-receptor.

Adipose Tissue↗
PubMed1976

Effect of the histamine (H2) inhibitor metiamide on histamine-stimulated bile flow in dogs.

The effects of the histamine H2-receptor inhibitor metiamide on histamine-stimulated canine bile flow and gastric hydrogen ion output were evaluated. Histamine was found to stimulate bile volume in doses comparable to those that stimulated gastric hydrogen ion output; both responses appeared to have the same maximal response dose, 150 mug/kg per h. Metiamide alone did not alter hepatic bile flow. Administration of metiamide, 2 mg/kg per h, along with various doses of histamine demonstrated that the H2-receptor antagonist decreased bile volume and gastric hydrogen ion output from values obtained with histamine administration alone. The D50 of histamine for bile flow was 16.3 mug/kg per h and the D50 for hydrogen ion output was 44.2 mug/kg per h, Kinetic analysis suggests that the decrease in histamine-stimulated hydrogen ion output produced by metiamide is the result of competitive inhibition; the decrease in histamine-stimulated bile volume by metiamide which is different from the hydrogen ion inhibition, suggests noncompetitive inhibition. These data indicate that the mechanism of histamine choleresis is different from the mechanism of histamine-stimulated gastric acid output and that histamine-stimulated bile flow may not be the result of direct hormone-receptor interaction.

Animals↗
PubMed1979

Metabolic studies on the uptake of [14C]-histidine and [14C]-histamine and histamine synthesis by guinea-pig basophils, in vitro.

The uptake of [14C]-histidine and [14C]-histamine and the conversion of [14C]-histidine to [14C]-histamine was measured in suspensions of guinea-pig bone marrow cells rich in basophils. When comparable amounts of labelled histidine or histamine were added to equal numbers of basophils, the uptake of histidine was approximately forty-five times greater than that of histamine. Purified eosinophils, neutrophils and mononuclear cells incorporated only a small proportion of [14C]-histidine when compared to the basophil; [14C]-histamine uptake by all these cell types was virtually negligible. Histidine uptake and the amount of histamine formed de novo was directly related to the number of basophils, the time of incubation and the substrate concentration. Histidine uptake was decreased by agents which inhibit glycolysis, oxidative phosphorylation, Na + - K + -dependent ATPase, protein synthesis and RNA synthesis. Inhibition was demonstrable in a dose-dependent fashion and at concentrations which had no apparent effect on cell viability. Inhibitors of DNA synthesis, and of microtubule function, had no influence on histidine uptake. Cytochalasin B, an inhibitor of microfilament function, also decreased histidine uptake but only at concentrations previously showen to affect hexose transport. None of the agents tested affected the uptake of [14C]-histamine or the amounts of new histamine formed from the histidine that had been incorporated. These studies suggest that histidine is preferentially incorporated into the basophil; that the uptake depends on the integrity of a number of metabolic pathways, but that once the histidine is taken up these requirements do not apply to the formation of new histamine. In contrast, histamine appeared to diffuse passively, and in relatively small amounts, into all the cell types tested.

Animals↗
PubMed1978

[Histamine and its role in peptic gastric diseases: the discovery of histamine-H2-receptor antagonists].

For the definition of histamine receptors the following prerequisites must be fulfilled: (1) Course of dose-response curves according to the mass-action law; (2) parallel displacement of these curves to the right in the presence of antagonists; (3) inhibition only by specific histamine antagonists; (4) slope of a Schild-plot not significantly different from unity. For H2-receptors these prerequisites could ideally be fulfilled, especially by the development of highly specific H2-receptor antagonists. However, this new class of compounds acts not only by mere competitive inhibition of histamine at its H2-receptor, but also by activating the metabolism of this secretagogue. A further explanation of the action of H2-receptor antagonists in the treatment of chronic duodenal ulcer may be given by studying the pathogenetic role played by histamine in the development of this disease: duodenal ulcer patients showed an increased liberation of histamine from mucosal mast cell stores as well as a decreased activity of histamine methyltransferase (i. e. longer action of histamine!). The rise in histamine content and histamine methyltransferase activity after vagotomy may be the basis for a biochemical explanation of the acid-reducing effect of this operation.

Animals↗
PubMed1975

The effects of the H1 and H2 antihistamines on "allergic" histamine release and its inhibition by histamine.

Antigen-induced, IgE-mediated release of histamine from human basophiles is an in vitro model of allergic reacttions; it is blocked by extracellular histamine, presumably as a result of its ability to increase adenosine 3',5'-monophosphate (cyclic AMP) levels. The H1 antihistamines do not antagonize these effects of histamine but at approximately equal to 1 mM cause histamine release and at approximately equal to 0.1mM inhibit antigen-induced histamine release. The phenothiazine antihistamines are 10-30 fold more potent inhibitors than the rest; other tricyclic antidepressant drugs share this activity. The mechanism of this inhibition, which occurs in both the 1 degree and 2 degree stages of histamine release, is not known but it is not due to partial agonist activity since the anti-H1 drugs cause a significant fall in cyclic AMP levels. The anti-anaphylactic effects of the H1 antagonists probably play no therapeutic role but we suggest that drugs structurally similar to the phenothiazine antihistamines should be developed for clinical testing. The H2 antihistamines block histamine-induced inhibition of histamine release and the increase in cyclic AMP levels, but neither cause nor inhibit histamine release. The K-B values for the anti-H2 drugs (burimamide approximately equal to 5 muM); metiamide approximately equal to 0.5muM); are similar to those described for other H2 receptors.

Animals↗
PubMed1977

Automated histamine analysis for in vitro allergy testing. II. Correlation of skin test results with in vitro whole blood histamine release in 82 patients.

The recently developed sensitive, automated histamine assay system was applied for in vitro allergy testing. The simplified method for histamine release from whole heparinized blood was used. Aliquots of blood and allergen were incubated for one hour at 37 degrees C, and each supernatant was then analyzed for histamine release. Nine common pollen and environmental allergens were used at three 10-fold dilutions for in vitro testing with the use of 20 ml of blood. Intradermal skin tests were correlated with the whole blood histamine release in 82 patients who had received no immunotherapy. A scoring system for the histamine results was developed to take into consideration the results with multiple allergen concentrations. When the skin test was strongly positive (greater than or equal to 3 + at 100 protein nitrogen units [PNU]/ml), the whole blood histamine release was positive in 89% of the tests. In contrast, when the skin test was negative ( less than 1 + at 100 PNU/ml), the histamine release was also negative in 99.8% of the cases. When the skin test was 1 +, the histamine release from whole blood was positive in 6% of the tests; and when the skin test was 2+, the whole blood results were positive in 32%. The accuracy, precision, and sensitivity of the automated histamine assay allow its application for the clinical study of allergic patients.

Allergens↗
PubMed1979

Early effects of corticosteroids on basophils, leukocyte histamine, and tissue histamine.

The comparative effect in 11 atopic subjects of a single intravenous injection of methylprednisolone on sequential studies of blood eosinophils, basophils, leukocyte sensitivity to antigen for histamine release, leukocyte histamine content, and skin histamine was examined. No significant changes occurred in any parameter after placebo treatment. In contrast, 4 hr after intravenous treatment with steroid there were significant decreases in mean eosinophil counts (-95%), basophil counts (-72%), and histamine content of 1 X 10(7) leukocyte samples (-62%). Temporal changes in the latter paralleled alterations in circulating basophil levels. No significant changes occured in the antigen histamine release sensitivity, or the total skin histamine. Studies over a longer period after steroids in 4 subjects showed eosinophil and basophil levels at a nadir at 8 hr, remaining suppressed for 24 hr, and returned to pretreatment levels by 72 hr. Results suggest that corticosteroids induce a prominent decrease in leukocyte histamine due to a depletion of basophils without a decrease in histamine content per basophil, and that skin tissue histamine stores remain unchanged by such treatment.

Basophils↗
PubMed1977

A simplified method for measuring basophil histamine release and blocking antibodies in hay fever patients. Basophil histamine content and cell preservation.

A simplified method for measuring basophil histamine release in grass pollen hay fever patients has been developed. Leukocytes were challenged in vitro with extracts of Phleum pratense (timothy) and the release of histamine was determined indirectly as the residual histamine in the cell sediment. Several steps to purify histamine thus became superfluous and histamine was directly conjugated with o-phthaldialdehyde to form a fluorophore. The simplified method showed a basophil histamine content which was in accordance with results obtained by more specific methods. No difference in basophil histamine content was found between normal and allergic persons. For the histamine liberation assay blood could be adequately preserved for transport for 48 h at room temperature by adding cell culture medium. Basophil histamine release technique allows evaluation of cell sensitivity for determination of the degree of allergy as well as the level of blocking antibodies.

Adult↗
PubMed1978

Central cardiovascular actions of histamine in rats: involvement of histamine H2-receptors.

Centrally induced pressor effects, associated with tachycardia have previously been demonstrated after intraventricular (i.c.v.) injections of histamine. The selective histamine H2-receptor agonists dimaprit (1--500 microgram) and 4-methyl histamine (1--10 microgram), and the histamine H1-receptor agonist 2-methyl histamin (1--10 microgram) elicited rises in blood pressure and heart rate after i.c.v. administration in urethane-anaesthetised rats. Metiamide (400--800 microgram, i.c.v.) antagonised the cardiovascular responses induced by dimaprit and 4-methyl histamine, but not the responses induced by 2-methyl histamine. In contrast mepyramine (100 microgram, i.c.v.) failed to antagonise the dimaprit-induced effects. It is concluded that histamine H1 and H2-receptors are present in the central nervous system of rats. Selective stimulation of either H1- or H2-receptors can lead to pressor effects associated with tachycardia after i.c.v. administration of specific agonists in urethane-anaesthetised rats. These responses are selectively antagonised by the respective receptor antagonists.

Animals↗
PubMed1978

A relatively specific and quantitative assay for histamine H2-receptor blocking activity by determination of inhibition of histamine-induced gastric acid secretion in the rat.

A relatively specific method for the quantitative assay of histamine H2-receptor antagonists has been developed. The method is based on the antagonism of the histamine-induced, and the spontaneous, gastric acid secretion in the stomach-perfused, urethane-anesthetized acute rat. For the induced gastric acid secretion, the animal received two consecutive equal injections of histamine (2 mg/kg, intrajugularly), the second 1.7 h after the termination of the first histamine-induced acid hypersecretion. Atropine (5 mg/kg), chlorisondamine (2 mg/kg), imipramine (10 mg/kg) and tripelennamine (5 mg/kg), administered i.p., failed to inhibit the histamine-induced, or the spontaneous, gastric acid secretion. Metiamide inhibited the histamine-induced acid secretion (ED50 1.85 mg/kg, i.p.) and the spontaneous acid secretion (10 mg/kg, i.p.). These results suggest that in the rat model employed in this study, histamine and H2-receptors play a very important role in the regulation of the gastric acid secretion. Other mechanisms involving cholinergic tone, biogenic amine uptake and histamine H1-receptors do not seem to intervene.

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↗