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Results for “Histamine Agonists”

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At least 19 recordsLinked to original sources
PubMed1983

Release of prolactin and luteinizing hormone by histamine agonists in ovariectomized, steroid-treated rats under ether anesthesia.

Responses to histamine agonists administered intraventricularly under ether anesthesia were analyzed to evaluate receptor mediation in histamine stimulation of prolactin and LH release in ovariectomized, estradiol-progesterone-treated rats (OVX-E2P-treated rats). Prolactin release was markedly increased by the H2-histamine agonists, 4-methyl histamine and Dimaprit. These effects were antagonized by metiamide, an H2-blocking agent. The H1-histamine agonist, 2-(2-pyridyl)ethylamine (PEA) in high doses released prolactin and its effect was partially prevented by metiamide. Mepyramine, and H1-antagonist, did not exert any effect on the release of prolactin enhanced by the histamine agonists. LH release was significantly increased after 4-methyl histamine administration. Its effect was weak and was blocked by metiamide. Neither Dimaprit nor PEA exhibited action on plasma LH levels. The results obtained with histamine agonists suggest that histamine evokes prolactin release in OVX,E2P-treated rats through H2-receptors. At present, conclusions on H2-receptor mediation in LH release induced by histamine cannot be drawn from these results. The above-mentioned data, however, conclusively discard a significant participation of H1-receptors.

Animals↗
PubMed1997

An ab initio study of histamine agonists.

A systematic theoretical study on histamine agonists and their interaction with H1 and H2 receptor models has been carried out utilizing ab initio molecular orbital technique. The effect of substituents on histamine agonists' charge distribution and their agonistic activity has been studied in detail. Drug-receptor interaction models have been studied at the Hartree Fock level of theory with a split valence basis set keeping the cost and efficiency of the calculation in mind. The study indicates that the agonistic activity is controlled either by receptor conformation or by steric hinderances caused by the substituents. The monocationic form of histamine does not appear to be a necessity for a proton relay process which is similar to the one proposed earlier by Weinstein and coworkers. The study also indicates some importance of common cellular ions in neurotransmitter properties of histamine.

Histamine Agonists↗
PubMed1981

A modulation of the anaphylactic basophil histamine release by selective H2 histamine agonists.

Two selective H2-histamine agonists, dimaprit and impromidine, have been tested for their action on histamine release from human basophils and rat mast cells. IgE-mediated basophil histamine release was inhibited by stimulation of histamine H2-receptors. However, differences between the actions of both dimaprit and impromidine were noticed. Both impromidine and dimaprit had no specific effect on 48/80-induced histamine release from rat mast cells, although the latter in higher concentrations either slightly increased spontaneous histamine release or non-specifically inhibited compound 48/80-induced release. The results are consistent with the view that activation of adenylate cyclase via H2-histamine receptors might be an important regulatory mechanism of histamine release from human basophils but not from rat mast cells.

Allergens↗
PubMed1984

Induction of prolactin release by H1- or H2-histamine agonists in maturing male and female rats.

Previous evidence has shown that histamine (HA) increases prolactin (PRL) release in adult male and female rats. This response is depending on the age of the animals and some differences were appreciated between male and female rats. In addition, at 20 days of age the PRL response was greater than earlier ages. The purpose of the present communication was to study further this response and to define the type of HA receptor that may be involved in the mediation of this PRL response. Animals of both sexes, at 5 or 20 days of age, were injected into the lateral brain ventricles with three log-doses of histamine (HA), 2,2, pyridilethylamine (2 PEA, and H1-histamine agonist), 4 methyl-histamine (4 MHA, an H2-histamine agonist) or saline as control. Fifteen minutes later a sample of blood was taken from the jugular vein and plasma PRL levels were determined by RIA. In complete agreement with previous work, results obtained indicate that HA is able to induce an increased PRL release in 20-day-old animals. This response was not identical in rats of both sexes. Female rats appeared to be more sensitive to HA than male rats. 2 PEA, was not able to reproduce the response in male rats but it was effective in female animals. 4 MHA induced the response in both sexes in a similar way than HA. At 5 days of age in male rats HA had no effect on PRL release. In female rats, instead, only the greater dose was able to induce a small but statistically significant response. In general, nor 2 PEA or 4 MHA were able to stimulate the PRL release at this age. The present results suggest that H2-histamine receptors are present in male rats and in female animals both types of receptors may be involved in the control of PRL release.

Animals↗
PubMedDate not supplied

Inhibition of acetylcholinesterase by histamine agonists and antagonists.

The histamine H1 and/or H2-receptor agonists showed weak acetylcholinesterase inhibitory activity. Their dissociation constants (Kis and/or Kii) were 2-methyl histamine (Kis = 1751 mumol/l, s.e. = 163) less than 4-methyl histamine (Kis = 3551 mumol/l, s.e. = 414) less than dimaprit (Kis = 2931 mumol/l, s.e. = 605; Kii = 3668 mumol/l, s.e. = 901) less than histamine (Kis = 6480 mumol/l, s.e. = 1360). Both histamine H1 and H2-receptor antagonists showed stronger acetylcholinesterase inhibitory activity. Their dissociation constants were ranitidine (Kii = 1.56 mumol/l, s.e. = 0.14) less than oxmetidine (Kis = 14.7 mumol/l, s.e. = 1) less than mepyramine (Kis = 178 mumol/l, s.e. = 23; Kii = 440 mumol/l, s.e. = 98) less than cimetidine (Kis = 199 mumol/l, s.e. = 12; Kii = 827 mumol/l, s.e. = 126). Using the ROSFIT programs for fitting data to common enzyme kinetic models, the inhibition caused by histamine, 4-methyl histamine, 2-methyl histamine, oxmetidine and neostigmine was of the competitive type. Mepyramine, cimetidine and dimaprit appeared to exhibit the modern non-competitive type of inhibition with their primary action on the enzyme rather than on the enzyme-substrate complex. Ranitidine seemed to act on the enzyme-substrate complex rather than the enzyme, conforming to the uncompetitive inhibition model. The clinical implications of acetylcholinesterase inhibition by cimetidine and ranitidine are discussed.

Acetylcholinesterase↗
PubMed1984

Plasma vasopressin levels after I.C.V. infusion of histamine agonists in the conscious goat.

Histamine H1-agonists 2-pyridylethylamine (2-PEA) and 2-methylhistamine and H2-agonists 4-methylhistamine, dimaprit and impromidine were given i.c.v. to conscious goats and the release of arginine vasopressin (AVP) was measured. 2-PEA at very low doses (9 and 27 mumoles/animal, equivalent to H1-activity of about 0.5 and 1.5 mumoles histamine, resp.) significantly increased plasma AVP. The H2-agonists did not cause consistent changes in AVP even if their relative doses were higher. It is concluded that the vasopressin releasing effect of histamine is due to H1-receptor activation.

Animals↗
PubMed1982

Pharmacological modification of immunoregulatory T lymphocytes. I. Effect of adenosine, H1 and H2 histamine agonists upon T lymphocyte regulation of B lymphocyte differentiation in vitro.

Human peripheral blood T lymphocytes were fractionated according to the lability of their sheep red blood cell (E) receptors to theophylline. Theophylline sensitive (Ts) cells function as suppressors of pokeweed mitogen induced B cell differentiation into plasma cells, while theophylline resistant (Tr) cells function as helper/inducer cells in this reaction. The Ts fraction is enriched for cells bearing receptors for the Fc portion of IgG (RFc gamma) while the Tr fraction is depleted of RFc gamma bearing cells. Brief exposure of Tr cells to adenosine or impromidine, an H2 histamine agonist, cause a rapid increase in the number of Tr cells bearing RFc gamma and the development of radioresistant suppressor cell activity. The RFc gamma induced on Tr cells by adenosine or impromidine are more stable in culture than the spontaneously occurring RFc gamma on Ts cells. Ts suppressor activity is radiosensitive and exposure of Ts cells to 2(2-pyridyl)ethylamine, an H1 histamine agonist, results in a marked decrease in RFc gamma on Ts cells as well as loss of Ts suppressor activity. These data indicate that RFc gamma expression and the immunoregulatory function of T lymphocyte subsets may be modified by drugs acting upon adenosine, H1 and H2 histamine receptors.

Adenosine↗
PubMed1984

In vivo release by histamine agonists and antagonists of endogenous catecholamines in the cat hypothalamus.

The posterior hypothalamus of anaesthetized cats was superfused through a push-pull cannula with histamine agonists and antagonists and the release of endogenous catecholamines was determined in the superfusate. Hypothalamic superfusion with histamine, 2-methylhistamine (H1-agonist), dimaprit (H2-agonist) or metiamide (H2-antagonist) enhanced the release of the catecholamines dopamine, noradrenaline and adrenaline. The releasing effects of these substances depended on the presence of calcium ions. Superfusion with 2-pyridylethylamine (H1-agonist) was virtually ineffective, while superfusion with 2-thiazolethylamine (H1-agonist) enhanced the rates of release of noradrenaline and adrenaline without influencing the release of dopamine. Superfusion with mepyramine (H1-antagonist) inhibited the release of noradrenaline and adrenaline without affecting the release of dopamine. Hypothalamic superfusion with a concentration of procaine which was equi-anaesthetic to that of mepyramine was ineffective. Ranitidine (H2-antagonist) did not alter the rates of release of the catecholamines. The releasing effect of histamine was inhibited on hypothalamic superfusion with mepyramine and ranitidine. Ranitidine also inhibited the releasing effects of dimaprit and 2-methylhistamine thus indicating that the releasing action of the latter compound was mainly due to stimulation of H2-receptors. These data suggest that blockade of H1-receptors of the posterior hypothalamus reduces the release of noradrenaline and adrenaline, while stimulation of H1-receptors seems to increase the rates of release of these two catecholamines. Stimulation of H2-receptors enhances the release of all three catecholamines. Thus, dopaminergic neurones of the hypothalamus seem to possess H2-receptors, while noradrenergic and adrenergic neurones possess H1- and H2-receptors.

Animals↗
PubMed1987

Presynaptic and postsynaptic effects of histamine and histamine agonists in the superior cervical ganglion of the rat.

Extracellular and intracellular recording techniques were used to study the effects of histamine and the histamine agonists [impromidine (IMP) and 2-thiazolylethylamine (2-TH)] on synaptic transmission in the superior cervical ganglion of the rat in vitro. At the concentrations employed (up to 10(-5) M) these compounds did not produce detectable effects on the electrical properties of the postsynaptic neurons. Histamine produced a dose-dependent reduction in the amplitude of the extracellularly-recorded presynaptic and postsynaptic compound action potential. The H2 receptor agonist impromidine reduced only the postganglionic compound action potential. Cimetidine, a specific H2 receptor antagonist, produced parallel shifts in the log dose-response curves for impromidine. Impromidine also reduced the average size of the evoked excitatory postsynaptic potential. The reduction of the mean amplitude of the excitatory postsynaptic potential was due to a decrease in the amount of acetylcholine (ACh) liberated by each preganglionic volley (mean quantal content, m) and a diminution in quantal size. The H1 receptor agonist, 2-TH produced a dose-dependent increase in the presynaptic and postsynaptic compound action potential and in m. The increase in m was not associated with changes in quantal size. The H1 antagonists, pyrilamine and promethazine, did not prevent facilitation of ganglionic transmission induced by 2-TH. It is concluded that histamine H1 and H2 receptors exist on preganglionic axons, or terminals in sympathetic ganglia of the rat. Activation of H1 receptors facilitates release of ACh whereas H2 receptor activation results in depressed release.

Action Potentials↗
PubMed1991

Histamine agonists and antagonists.

The role of histamine in brain function is discussed. A brief review is presented on the three types of histamine receptors with regard to their biochemistry and functions. The agonists and antagonists of these three classes of histamine receptors are discussed, together with the role such compounds play in clinical therapy and pharmacology.

Animals↗
PubMed1976

Depression of rat cerebral cortical neurones by H1 and H2 histamine receptor agonists.

Histamine (H) and H1 agonists 2-pyridylethylamine (PEA) and 2-methylhistamine (2-MH) produced a greater depression of the corticospinal and unidentified rat cerebral cortical neurones than did 4-methylhistamine (4-MH), an H2 agonist. Mepyramine antagonized the effects of 2-MH, PEA and H, and partially antagonized the depression induced by 4-MH. Metiamide and cimetidine, H2 antagonists, blocked 4-MH and H but not 2-MH- and PEA-induced depression. These results indicate that H-induced depression of cortical neurones involves activation of H1 and H2 receptors.

Acetylcholine↗
PubMedDate not supplied

Liver alcohol and aldehyde dehydrogenase: inhibition and potentiation by histamine agonists and antagonists.

1. The in vitro effects of histamine, some other H1- and H2-receptor agonists and some antagonists were studied on the specific activities and kinetics of rat liver alcohol dehydrogenase (ADH), and cytoplasmic and mitochondrial liver aldehyde dehydrogenase (ALDH). 2. Histamine (H1- and H2-agonist) non-competitively inhibited ADH. There were no changes of cytoplasmic and mitochondrial liver ALDH activities in the presence of 2-(2-aminoethyl) pyridine. 3. Betazole (H2-receptor agonist) produced a competitive inhibition of mitochondrial ALDH but not of ADH or cytoplasmic ALDH. 4. Diphenhydramine (H1-receptor antagonist) non-competitively inhibited ADH at a lower concentration. It stimulated mitochondrial ALDH activity without changes in cytoplasmic ALDH from control values. 5. Burimamide (H2-receptor antagonist) produced a biphasic and dose-dependent stimulation and non-competitive inhibition of ADH and it non-competitively inhibited ALDH in both cytoplasmic and mitochondrial fractions. Metiamide (H2-receptor antagonist) non-competitively inhibited all ADH and ALDH of both liver fraction studied. 6. It is concluded that liver ADH and ALDH activity can be altered by compounds which affect both H1- and H2-histamine receptors and that these compounds may cause an in vivo potentiation and/or reduction of the toxic effect of ethanol.

Alcohol Oxidoreductases↗
PubMed1984

Effects of histamine agonists and antagonists on luminol-dependent chemiluminescence of granulocytes.

Histamine inhibited luminol-dependent chemiluminescence (CL) of granulocytes in a dose-dependent manner, with an ID50 of about 3 X 10(-5) M. Dimaprit, a selective H2-agonist, produced a histamine-like effect. Furthermore, cimetidine, ranitidine, and TZU 0460, which are selective H2-antagonists, but not mepyramine, a selective H1-antagonist, blocked the inhibitory effect of histamine on CL. Thus it may be concluded that the inhibitory effect of histamine is mediated via histamine H2-receptors. H1- and H2-antagonists per se, except at extremely high concentrations, had no effect on CL of granulocytes.

Cimetidine↗
PubMed1980

Specific activation of cyclic AMP-dependent protein kinase(s) by H2-histamine agonists in isolated gastric mucosal cells from guinea-pig.

Histamine stimulated cyclic AMP-dependent protein kinase activity in dispersed mucosal cells from guinea-pig gastric fundus (Ka = 5 microM). The H2-agonists dimaprit and impromidine produced similar effects, while the H1-agonist 2-(2-pyridyl) ethylamine had only a weak one. The H2-antagonist cimetidine competitively inhibited 0.1 mM histamine stimulation (Ki = 2 microM). In contrast, the H1-antagonist diphenhydramine had no effect up to 1 mM.

Animals↗
PubMed1981

Effect of histamine agonists and antagonists on the production of murine reaginic antibodies.

At least wo histamine receptors have been pharmacologically defined. Using the appropriate agonists and antagonists, the possible involvement of these receptor types in the production of reaginic antibodies in the rodent was investigated. After injecting mice with dinitrophenyl-ovalbumin (DNP-OA), maximal serum reaginic titers occurred on day 11 as measured by heterologous passive cutaneous anaphylaxis. If the mice were dosed daily (i.p.) with the H1 agonist, 2-methylhistamine, or the H2 antagonist, metiamide, the titers of reaginic antibodies on day 11 were significantly higher than the controls. The titers were significantly lower than the controls if an H2 agonist (4-methylhistamine, dimaprit, or impromidine) or if the H1 antagonist, pyrilamine, was administered daily. None of these agents significantly affected total serum IgG titers as measured by ELISA. However, if the mice were injected with DNP-OA on day 0, then dosed daily with metiamide, pyrilamine, or 4 methylhistamine beginning on day 32, the titers of reaginic antibodies elicited by a second injection of DNP-OA given on day 36 were not significantly different from the titers of the non-drug treated mice. Thus, under these conditions, with these agents, the results suggest that histamine receptors may be involved in modulating the production of reaginic antibodies during a primary immunological response, H1 receptor agonists enhanced, while H2 receptor agonists suppressed the responses, and the reverse effect was observed with the appropriate antagonists. However, histamine receptors appear not to be measurably involved in the development of the secondary reaginic response.

Animals↗
PubMed1981

Histamine agonist and antagonist drugs: interference with CNS control of GH release in rats.

The effects of the administration into the brain ventricle of histamine, selective H1- and H2-receptor agonists and antagonists and chemically similar substances with nonspecific activity on basal and morphine-stimulated growth hormone (GH) secretion in normal male rats were studied. None of the drugs had any significant effect on baseline rat GH levels, but histamine and H1 agonists were able to decrease the rat GH release evoked by morphine. Mepyramine (H1 antagonist) had no consistent effect by itself but was effective in preventing the inhibitory action of 2-methylhistamine (H1 agonist). H2 agonists and antagonists and their chemical analogues were all inhibitory, but by a mechanism which is nonspecific and must be interpreted cautiously. These results confirm the inhibitory effect of histamine on rat GH release and indicate that H1 receptors in the CNS are responsible for this effect.

Animals↗
PubMed1983

Effects of histamine agonists and antagonists (H1 and H2) on ganglionic transmission and on accumulation of cyclic nucleotides (cAMP and cGMP) in rat superior cervical ganglion in vitro.

Histamine and 4-methylhistamine inhibited ganglionic transmission in the rat superior cervical ganglion in vitro via H2-histaminergic receptors. Under blockade of H2-receptors, 4-methylhistamine sometimes showed slight facilitation of ganglionic transmission, when repetitive stimuli were applied. The H1-receptor agonist, 2-pyridylethylamine, was ineffective. Histamine and 4-methylhistamine increased both cyclic AMP (cAMP) and cyclic GMP (cGMP) levels in concentrations depressing ganglionic transmission, whereas 2-pyridylethylamine increased only cAMP concentrations in the isolated ganglia. Histamine-induced accumulation of cyclic nucleotides was only partially prevented by either histamine--H1- and H2-receptor antagonists, but abolished by their combination. It is concluded that changes in intraganglionic cyclic nucleotides induced by histaminergic receptor agonists did not apparently correlate with their effect on ganglionic transmission in vitro.

Action Potentials↗