Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HISTAMINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources
PubMedDate not supplied

Involvement of histamine receptors in mediation of histamine induced thermoregulatory response in rats.

At there ambient air temperature range, the rectal temperature changes following infusion of histamine either into lateral ventricle (L.V.) or IVth ventricle (IVth V) were studied. At an ambient temperature range of 19-22 degrees C, hypothermia occurred following histamine infusion either into L.V. or IVth V. Hypothermia elicited from infusion of histamine into L.V. was prevented with pretreatment of H1-receptor blocker (mepyramine), but in case of IVth V, it was prevented with H2-receptor blocker(cimetidine). These H1 and H2-receptor antagonists were ineffective in preventing hypothermia following histamine infusion into either L.V. or IVth V, when the ambient air temperature was maintained low (11-13 degrees C).

Animals↗
PubMed1979

Relaxant action of histamine on rabbit trachea: possible existence of third histamine receptor subtype.

The carbachol contracted rabbit trachea relaxes to isoproterenol, PGE1, E2, histamine and bradykinin. Histamine-induced relaxations were resistant to mepyramine (an H1-antagonist), burimamide, cimetidine, metiamide (H2-antagonists), propranolol (a beta-adrenoceptor blocker), indomethacin (a potent inhibitor of prostaglandin synthesis), trasylol (an inhibitor of kallikreins), aminophylline (a purinergic receptor blocker) and dibenzyline (a "D"-tryptamine receptor antagonist). The evidence achieved with these pharmacological agents appears to suggest that the chemical mediator responsible for the relaxant response to histamine is unlikely to be: catecholamines, prostaglandins, 5-HT, adenosine or ATP or kinins. The existence of H2-(iso or H3) histamine receptor subtype in rabbit trachea is postulated.

Airway Resistance↗
PubMed1982

Influence of ultraviolet light on itch and flare reactions in human skin induced by histamine and the histamine liberator compound 48/80.

The itch and flare responses induced by intradermal injection of histamine and the histamine liberator compound 48/80 were studied in healthy volunteers before and after exposure to UVB, UVA or PUVA administered 2-3 times weekly for 4 weeks. All three modalities were found to inhibit the responses induced by compound 48/80. The degree of tanning was most pronounced after PUVA and weakest after UVB, without any correlation between tanning and inhibition of itch. In contrast, when induced by histamine, the responses were not inhibited to the same extent, pronounced and significant inhibition being observed only for itching in subjects exposed to UVB. It is concluded that UVB, UVA and PUVA all might be of benefit in treating pruritic states if histamine release is involved and that UVB might have an additional effect by inducing hyposensitivity to itching stimuli.

Adult↗
PubMed1982

Diurnal variations in brain and pituitary histamine and histamine-N-methyltransferase in the rat and guinea pig.

The circadian variation of histamine concentrations and histamine-N-methyltransferase (E.C. 2.1.1.8., HNMT) activities were measured in different parts of rat and guinea pig brain and pituitary glands after an adaptation to a daily 12-hour light and 12-hour dark schedule. A significantly higher histamine content was found in rat hypothalamus at 19.00 hours, at the end of the light period, then a decline during the dark hours followed by an increase during the daytime. No similar changes were seen either in the other parts of the brain or in the pituitary gland. In the guinea pig hypothalamus a somewhat reverse pattern of histamine content was seen as compared to that in the rat, the peak occurred at 8.00 hours and the lowest level at 14.00 hours. In other parts of the brain the changes were not significant. In rat hypothalamus there were also significant changes in HNMT activities, with a higher level during darkness. In the guinea pig, the HNMT activities were much higher than in the rat, and in hypothalamus, cortex and striatum there was a modest increase at 2.00 hours, with another upward trend at 14.00 hours. It will be of interest to see whether or not these species differences reflect different circadian activity rhythms and/or different living habits of these two species, and with which physiological functions they may be connected.

Animals↗
PubMed1980

Effects of histamine and histamine antagonists on the uptake and release of catecholamines and 5-HT in brain synaptosomes.

The effect of histamine and histamine antagonists on the uptake and release of monoamines was studied using rat brain synaptosomes. For uptake experiments, P2-synaptosome fractions were incubated in buffer for 2 min in the presence of tritiated dopamine, noradrenaline or 5-hydroxytryptamine (5-HT) and the inhibitor studied. Only an /H1-antagonist mepyramine (pyrilamine) inhibited monoamine uptake at reasonable concentrations. For release experiments, preloaded synaptosomes were incubated with the substanances to be studied for 2 or 5 min in buffer, and the decrease in radio-activity assayed and compared with synaptosomes incubated with the solvent. Only histamine caused some release, but the concentration range necessary to cause a similar level of release was at least one hundred times greater than that of tyramine. Hence it is unlikely that H2-antagonists would exert their pharmacological effects in the central nervous system by inhibiting monoamine uptake or by causing a tyramine-like releasing effect. Also histamine is necessary at very high concentrations before such secondary effects are likely.

Animals↗
PubMed1993

[Inhibitory effects of Reitakutuukitokasin'i on the antigen-antibody reaction in rats investigated by measuring the increase in blood histamine level and the histamine release from peritoneal mast cells].

The antiallergic effects of Reitakutuukitokasin'i (RKS) on the increase in blood histamine level by antigen challenge were investigated in actively sensitized rats in comparison with those of azelastine and disodium cromoglycate (DSCG). The increase in blood histamine level after a systemic anaphylactic reaction elicited by intravenously injected antigen (egg albumin) was significantly inhibited by oral and intravenous administrations of RKS and azelastine or DSCG. Namely, RKS at 50 and 100 mg/kg (p.o.) caused 17% and 28% inhibition, respectively, and azelastine at 5 and 10 mg/kg (p.o.) caused 28% and 29% inhibition, respectively. RKS at 0.1 and 0.5 mg/kg (i.v.) caused 33% and 29% inhibition, respectively, and DSCG at 10 mg/kg (i.v.) caused 53% inhibition. However, large doses of RKS (500 mg/kg, p.o., 2.5 and 10 mg/kg, i.v.) caused no significant inhibition. The histamine release from rat peritoneal mast cells (RPMC) by antigen-antibody reaction was also investigated, and proved to be inhibited significantly by RKS. Namely, RKS at 5 x 10(-4), 10(-3) and 2 x 10(-3) g/ml caused 42, 71 and 79% inhibition, respectively. These results suggest that RKS is an antiallergic drug similar to azelastine and DSCG with a common inhibitory action on the release of histamine.

Anaphylaxis↗
PubMed1993

Effect of the novel histamine H2-antagonist 5,6-dimethyl-2-[4-[3-(1- piperidinomethyl)phenoxy]-(z)-2-butenylamino]-4(1H)-pyrimidine dihydrochloride on histamine-induced gastric acid secretion in Heidenhain pouch dogs.

Effects of IGN-2098 (5,6-dimethyl-2-[4-[3-(1-piperidinomethyl)phenoxy]- (z)-2-butenylamino]-4(1H)-pyrimidone dihydrochloride, CAS 126869-04-3) a novel histamine H2-antagonist, on histamine-induced gastric acid secretion were investigated in Heidenhain pouch dogs in comparison with those of famotidine, roxatidine acetate HCl and cimetidine. Orally administered IGN-2098 (0.03-1.0 mg/kg), famotidine (0.01-0.3 mg/kg), roxatidine acetate HCl (0.1-1.0 mg/kg) and cimetidine (0.3-3.0 mg/kg) showed dose-dependent inhibition on histamine-induced gastric acid secretion, and ED50 values of IGN-2098, famotidine, roxatidine acetate HCl and cimetidine were 0.077, 0.024, 0.200 and 0.585 mg/kg, respectively. IGN-2098 was effective even at 6 h after administration and ED50 value was 0.315 mg/kg. IGN-2098 was effective also by intravenous route. The inhibitory effect of IGN-2098 on histamine-induced gastric secretion was not affected by the repeated administration of IGN-2098 (1 mg/kg b.i.d. for 14 days). These results show that IGN-2098 is a potent and long acting antisecretory agent and is a useful antisecretory drug for the treatment of peptic ulcer disease.

Administration, Oral↗
PubMed1993

New activation model for the histamine H2 receptor, explaining the activity of the different classes of histamine H2 receptor agonists.

Recently we developed amthamine [2-amino-5-(2-aminoethyl)-4-methylthiazole]. This cyclic analogue of dimaprit proved to be the most potent and selective histamine H2 receptor agonist of a series of substituted 4- or 5-(2-aminoethyl)thiazoles. Quantum chemical studies on histamine (N pi-H tautomer), dimaprit, and amthamine revealed that, based upon geometries of molecular electrostatic potentials, it is likely that these agonists accept a proton from the proton-donating receptor site on their double-bonded (heteroaromatic) nitrogen atoms. In contrast to reported models, this new model is able to accommodate and explain the agonistic activities of all known (including nontautomeric) histamine H2 receptor agonists. Quantitative structure-activity relationship studies with a series of substituted histamine derivatives and heterocyclic analogues support the presented model, in which the monocations in extended conformation interact with the receptor surface; their affinities correlate with the proton association constants of the heteroaromatic nuclei. The negatively charged anchoring site for the ethylammonium side chain of these agonists in this model is a functional group with a pKa value of 4.17.

Histamine↗
PubMed1998

Effects of inhaled KAA-276, a selective histamine H1 receptor antagonist, on antigen- and histamine-induced bronchoconstriction in animals.

The antiasthmatic profile of KAA-276 (1-[1-(4-fluorophenylmethyl)-1H-benzimidazole-2-yl]-5-[2-[4-(2- carboxethyl) phenyl]ethyl]-1,5-diazacyclooctane sulfate, CAS 167264-26-8), a newly synthesized histamine H1 receptor antagonist, given by inhalation as an aerosol was investigated and compared with the profiles obtained using other routes of administration. When given by inhalation, or by intravenous or oral routes, KAA-276 inhibited antigen-induced bronchoconstriction in rats with ID50 (a dose to inhibit the antigen-induced response by 50%) values of 0.054%, 1 mg/kg, and 51.2 mg/kg, respectively. KAA-276 prevented the histamine-induced wheal reaction in rats dose-dependently with ID50 values of 0.22% by inhalation, 0.18 mg/kg by the intravenous route, and 2.3 mg/kg by the oral route. To judge from these results, inhaled KAA-276, unlike intravenous or oral KAA-276, had no inhibitory effect on the histamine-induced wheal reaction at a dose (0.054%) that is effective against the antigen-induced airway asthmatic response. Inhaled KAA-276 suppressed antigen-induced bronchoconstriction in actively sensitized guinea pigs, and histamine-induced bronchoconstriction in monkeys. These results suggest that inhalation of KAA-276 would benefit patients with bronchial asthma without inducing unwanted systemic effects.

Administration, Inhalation↗
PubMed1981

The role of histamine in wound healing. II. The effect of antagonists and agonists of histamine receptors (H1 and H2) on collagen levels in granulation tissue.

The effects of mepyramine (H1-receptor antagonist), cimetidine (H2-receptor antagonist), IEM-813 (H1-receptor agonist) abd 4-Met-Hi (H2-receptor agonist) on collagenogenesis processes in subcutaneous implanted sponges of rats were studied. Administration into sponges of cimetidine 30 min before histamine injection blocked both the stimulatory effect of low histamine doses and the inhibitory effect of high histamine doses of collagen formation. Low doses of 4-Met-Hi increased collagen levels but reduced the levels at high doses. Mepyramine and IEM-813 did not influence collagen biosynthesis.

Animals↗
PubMed1986

Biochemical and pharmacological characterization of histamine-mediated up-regulation of human platelet serotonin uptake. Evidence for a subclass of histamine H2 receptors (H2h) highly sensitive to H2 receptor antagonists.

The stimulatory effect of histamine: H (1.2 to 3-fold increase) on serotonin (5-HT) uptake by human platelets was observed after a 5 min incubation period in the presence of 2.5 X 10(-7) M histamine, followed by subsequent 5 min incubation of the platelets with 10(-7) M [3H] 5-HT. Methyl, ethyl and acetyl substituents in the side chain of H mimicked the stimulatory effect of H. In contrast, H analogs methylated at the position N-1 of the imidazole ring of H, as well as imidazole and histidine inhibited platelet 5-HT uptake. The cAMP-inducing agents forskolin and theophylline have no effect on 5-HT uptake when they are tested alone or in combinations with H. In contrast, the cGMP-inducing agent sodium nitroprusside (10(-7) M-10(-6) M) stimulated and potentiated H-mediated up-regulation of 5-HT uptake. Histamine H2 receptor agonists and antagonists are more potent than drugs acting on H1 receptors (H2 greater than H1). However, the inhibition constants Ki are not consistent with those determined for typical H1, H2, H3 receptors characterized in other tissues. This findings provide further evidence for the existence of multiple forms of H receptors and suggest the involvement of a subpopulation of H2 receptors, highly sensitive to H2 receptor antagonists (H2h), mediating 5-HT uptake in human platelets.

Blood Platelets↗
PubMed1980

Influence of histamine or dimaprit on histamine release induced by anti-ige from human whole blood.

In human subjects histamine release from whole blood by anti-IgE and studied under several concentrations of histamine and dimaprit. The results obtained in our experiments led us to question the autoregulatory feed-back mechanism postulated by BOURNE et al. [1]. Apparently this mechanism does not apply for all patients particularly at doses which resemble physiological concentrations of histamine.

Antibodies↗
PubMed1981

Brain histamine H1- and H2-receptors and histamine-sensitive adenylate cyclase: effects of antipsychotics and antidepressants.

Several classes of psychoactive compounds have been investigated for their effects on histamine-sensitive adenylate cyclase in cell free preparations from the guinea-pig cerebral cortex. Their inhibitory actions on this enzyme system have been compared with their abilities to displace [3H]pyrilamine and [3H]cimetidine from histamine H1- and H2-receptor sites, respectively. The results of these studies show that compounds which inhibited the histamine-sensitive cyclase were also displacers of either ([3H]pyrilamine or [3H]cimetidine or both 3H]ligands from their binding sites. In spite of the lack of a correlation between binding and cyclase antagonism, it was observed that compounds that displace both ligands showed greater inhibition of the cyclase than those that have affinities for sites labeled by one or the other ligand. It was concluded that antihistamines, the antipsychotics and the antidepressants share a common property through their antagonism of H1-receptors and that may be responsible for their sedative side effect.

Adenylyl Cyclases↗
PubMed1986

Histamine in dorsal and ventral hippocampus. II. Effects of H1 and H2 histamine antagonists on exploratory behavior in male rats.

The effects on Hole-Board behavior of histamine (HA) microinjected into different parts of the hippocampus and the effects of pyrilamine (PYR, an H1-histamine antagonist), ranitidine (RAN, an H2-histamine antagonist) or alpha-fluoromethyl-histidine (alpha-FMH, an irreversible inhibitor of the HA synthetizing enzyme) injected into the hippocampus on behavior were studied. Forty five nMol of HA were injected stereotaxically into the dorsal or ventral hippocampus. Five min later, Hole-board behavior was measured. It was observed that HA inhibited locomotion and rearing only in the rats injected into the ventral hippocampus. In other experiments, animals were microinjected into the ventral hippocampus with 135 nMol of PYR or RAN in 1 microliter of saline solution. Ten min later, they were microinjected with 45 nMol of HA. Hole-board exploratory activity was measured 5 min thereafter. Results showed that both PYR and RAN were effective in counteracting the inhibitory effect of HA on locomotor activity, but only RAN was able to block the inhibitory action of HA on rearing behavior. Head-dipping frequency was not affected by these treatments. In rats microinjected with 20 nMol of alpha-FMH, increased scores of locomotion were observed but the other behaviors (head-dipping frequency, grooming and rearing) were not affected. The present results support the hypothesis that HA in hippocampus may be exerting a regulatory role on behavior by interaction with H1 and H2 receptors.

Aminopyridines↗
PubMed1995

Does histamine stimulate cyclic AMP formation in the avian pineal gland via a novel (non-H1, non-H2, non-H3) histamine receptor subtype.

The effects of histamine (HA) and selective HA H1-, H2 and H3-receptor agonists on cyclic AMP formation were investigated in intact chick and duck pineal glands HA potently stimulated the pineal cycle AMP formation. The effect of HA was mimicked fully by N alpha-methylated histamines, and partially by several histaminergic drugs: 2-thiazolylethylamine (H1) amthamine (H2) and R alpha-methyl-histamine (H3). Dimaprit, another selective H2-agonist showed marginal activity. Forskolin highly potentiated the action of HA, and only weakly affected the effects of 2-thiazolylethylamine and amthamine. In the chick pineal, the stimulatory effects of HA and the tested histaminergic drugs were not blocked by mepyramine and thioperamide (H1- and H3-blockers, respectively), but they were antagonized by H2-receptor selective compounds ranitidine and aminopotentidine, which, however, acted in a noncompetitive manner. Another H2-selective blocker zolantidine antagonized the HA effect only when used at very high (30-100 microM) concentrations. In the duck pineal, the stimulatory effect of HA on cyclic AMP production was unaffected by mepyramine (H1), thioperamide (H3), and ranitidine (H2), and only partially inhibited by the H2-blocker aminopotentidine. Electrophysiological experiments revealed that HA is capable of evoking inward currents in most of the tested cells acutely isolated from chick pineal gland. The present findings further indicate that the pharmacological profile of the avian pineal HA receptor, whose stimulation leads to activation of cyclic AMP production, is different from any known HA receptor type (H1, H2, H3), and suggest the existence of either an avian-specific HA receptor, or a novel HA receptor subtype. Electrophysiological data suggest that the pineal HA receptor may be somehow linked to activation of an ionic channel.

Animals↗
PubMed1985

H2 histaminic receptors in rat cerebral cortex. 2. Inhibition of [3H]histamine by H2 antagonists.

Sites labeled by [3H]histamine in homogenates of rat cerebral cortex reveal a pharmacological specificity typical of H2 receptors. Fourteen H2 antagonists inhibit the specific binding of the radioligand to the same level; Hill coefficients are near or equal to one for five compounds and markedly lower for nine. The binding patterns of individual antagonists (A) are well described by the empirical expression Y = F1K1/(K1 + [A]) + F2K2/(K2 + [A]), in which F1 and F2 sum to 1; F2 is 0 for those drugs that reveal a Hill coefficient of 1. Concentrations of A that reduce specific binding by 50% (IC50) correlate well (r = 0.991; P less than 0.00001) and show good numerical agreement with potencies reported for inhibition of the response to histamine in H2-mediated systems. The correlation is poorer when IC50 is replaced by either K1 (r = 0.973) or K2 (r = 0.921) for those antagonists that reveal both; the antihistaminic activity of the drug thus appears not to be associated preferentially with one or other class of sites. Since F2 varies from 0.16 to 0.60 among those antagonists that discern heterogeneity, the antagonist appears to determine the distribution of sites between the two classes. Moreover, a correlation among antagonists between values of K1 and K2 (r = 0.975; P = 0.00001) suggests that the apparent heterogeneity reflects different conformers within an otherwise homogeneous population. H2 antagonists appear to be noncompetitive with respect to each other and to the radioligand: one antagonist has relatively little effect on the values of K1, K2, and F2 revealed by another; also, estimates of K1 and K2 are independent of the concentration of [3H]histamine between 1.3 and 10 nM, although the radioligand exhibits an apparent dissociation constant of 3.9 nM [Steinberg, G. H., Eppel, J. G., Kandel, M., Kandel, S. I., & Wells, J. W. (1985) Biochemistry (preceding paper in this issue)].

Animals↗
PubMed2002

Histamine h(4) and h(2) receptors control histamine-induced interleukin-16 release from human CD8(+) T cells.

Histamine is known to trigger the release of interleukin (IL)-16 from human CD8(+) cells. However, the individual roles of the presently known histamine receptor subtypes (H(1)-H(4)) in this inflammatory response have not been fully characterized. Histamine stimulation of human CD8(+) T lymphocytes purified from peripheral blood led to a 5- to 8-fold increase in the basal release of IL-16 within 24 h, and this increase was significantly blocked by the H(2)-selective antagonist, cimetidine, or by thioperamide, an antagonist of H(3) and H(4) receptors, respectively. The H(1) antagonist pyrilamine showed limited effects. Agonists selective for H(2) (dimaprit), H(3/4) (R-(-)-alpha-methylhistamine), and H(4) (clobenpropit) were capable of inducing the release of bioactive IL-16 because CD8(+) cell supernatants induced CD4(+) cell migration, which was abrogated by an anti-IL-16 antibody. Furthermore, preincubation of lymphocytes with pertussis toxin abolished IL-16 release triggered by activation of the G(i/o)-coupled H(4) receptor but not by the H(2) receptor. Messenger RNA expression studies confirmed H(4), H(2), and H(1) expression in human CD8(+) lymphocytes, whereas H(3) mRNA was completely absent. All leukocyte populations investigated expressed mRNA for H(4), with highest levels found in eosinophils, dendritic cells, and tonsil B cells. H(4) expression was also detected in human lung, trachea, and various cells of human lung origin, such as fibroblasts, bronchial smooth muscle cells, epithelial, and endothelial cells. Since many of those are known sources of IL-16, immune cell- and lung cell-expressed H(4) receptors may have a general role in the control of this mediator of inflammatory disorders such as asthma.

Base Sequence↗
PubMed2003

The histamine H2-receptor antagonist, cimetidine, inhibits the articular osteopenia in rats with adjuvant-induced arthritis by suppressing the osteoclast differentiation induced by histamine.

The effects of cimetidine on rat adjuvant arthritis (AA) and rat osteoclast differentiation were studied. For the in vivo experiments, AA was induced by injections of Mycobacterium tuberculosis H37RA either subcutaneously into the base of the tail or into the right hind paw. The osteoclast differentiation was assessed by estimating the number of tartrate-resistant acid phosphatase-positive multinuclear cells in the bone marrow culture. Cimetidine, at the dose of 25 mg/kg body weight, reduced the paw swelling by 70% (P<0.01). Cimetidine, at 10 microM concentration, inhibited 1,25-dihydroxyvitamin D(3) (1,25[OH](2)D(3)) and histamine mediated osteoclast differentiations by 40% (P<0.01) and 60% (P<0.001), respectively. Dimaprit, at 0.3 microM, stimulated the cell differentiation by 100% (P<0.01). Mepyramine reduced osteoclast differentiation, but the reduction was not statistically significant. Measurements of bone mineral density of the femur indicated that 5 mg/kg of cimetidine treated animals had 30% (P<0.01) higher mineral density in comparison with that of the AA control group that received no cimetidine. These results suggest that histamine is a potent inducer of osteoclast differentiation, at least in part, through the histamine H(2)-receptor, and cimetidine has a preventive effect on articular destruction and accompanying inflammation in arthritic rats. These observations may provide critical insights into the pathogenesis of the bone pathology seen in patients with RA.

Animals↗