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K Maeyama

Publications and source records attributed to K Maeyama.

At least 91 records · Page 5Linked to original sources
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↗
PubMed1988

Regional changes in brain histamine levels following dietary-induced thiamine deficiency in rats.

Histamine levels in thiamine deficient rats were significantly lower in the hippocampus, amygdala, olfactory bulb, thalamus and pons-medulla oblongata than those of normal and pair-fed groups. In the case of the hypothalamus, thiamine deficiency produced a significant increase in histamine levels. These changes observed in the thiamine deficient group were reversed to the normal levels by supplying the normal diet. These data present a new finding that thiamine deficiency affects the central histaminergic neuron system as well as other monoaminergic systems.

Animals↗
PubMed1987

The kinetics of phosphoinositide hydrolysis in rat basophilic leukemia (RBL-2H3) cells varies with the type of IgE receptor cross-linking agent used.

We have re-examined, by high pressure liquid chromatographic (HPLC) procedures, the hydrolysis of 3H-labeled inositol phospholipids in rat basophilic leukemia (RBL-2H3) cells. Previous studies showed no clear correlation between the release of any particular inositol metabolite and the calcium signal in these cells. Paradoxically no responses were observed when the cells were stimulated with the antigen, aggregated ovalbumin, in the absence of external Ca2+. We report here that in the absence of external Ca2+ aggregation of the IgE receptor by agents other than aggregated ovalbumin causes the release of small amounts of [3H]inositol phosphates and a small increase in levels of cytosol Ca2+ (approximately 25 nM). The response, however, varied with the type of stimulant used. Within seconds after addition of 24 mol of dinitrophenol conjugated with 1 mol of bovine serum albumin to cells primed with dinitrophenol-specific IgE there was a small burst in release of [3H]inositol 1,4,5-triphosphate, [3H]inositol 1,3,4,5-tetrakisphosphate, and [3H]inositol 1,3,4-trisphosphate which was followed by a gradual rise in inositol 1,3,4-trisphosphate, inositol bisphosphate, and inositol monophosphate. Eventually, all inositol phosphates reached different steady state levels which were maintained for at least 40 min. In contrast, the initial response to oligomeric IgE, which aggregates receptors at a relatively slow rate, was muted although the subsequent development of the response was the same. The levels of inositol pentakisphosphate and hexakisphosphate remained unchanged. These and other studies with cell extracts support the conclusion that inositol 1,4,5-trisphosphate, a putative messenger for release of intracellular Ca2+, was converted to inositol 1,3,4,5-tetrakisphosphate and thence to inositol 1,3,4-trisphosphate. Both trisphosphate metabolites were dephosphorylated in sequential fashion by phosphatase enzymes in the cytosolic and membrane fractions. However, the appearance of several isomers of inositol monophosphates and bisphosphates suggested that degradation proceeded through multiple pathways in the intact cell.

Animals↗
PubMed1986

Loss of secretory response of rat basophilic leukemia (2H3) cells at 40 degrees C is associated with reversible suppression of inositol phospholipid breakdown and calcium signals.

Antigen-induced stimulatory signals as well as histamine secretion from the RBL-2H3 cells were found to be highly temperature dependent. There was no hydrolysis of inositol phospholipids, increase in cytosol calcium concentration (calcium signal), or secretion upon antigen stimulation at temperatures below 20 degrees C. At higher temperatures (i.e., 20 to 37 degrees C), all responses increased in extent with increase in temperature. Temperatures of 38 degrees C or higher, however, resulted in a marked decline in all responses, until no responses were observed at 40 to 42 degrees C. As indicated by the decay in calcium signal, the duration of response was also temperature dependent. The response was of long duration at 30 to 32 degrees C, but it became progressively more transient as the temperature was increased from 32 to 40 degrees C. The effects of low or high temperature were fully reversible. For example, in the presence of antigen, stimulatory signals immediately appeared once the temperature was decreased from 40 to 37 degrees C. Although the diminished responses could be explained, in part, by a reduction in rates of IgE receptor aggregation and phospholipase C activity, the reductions were insufficient to account for complete loss of activity at 40 degrees C. We conclude that generation of intracellular signals in 2H3 cells is blocked by quite small elevations in temperature above 37 degrees C, possibly as consequence of changes in membrane fluidity.

Animals↗
PubMed1986

Quantitative relationships between aggregation of IgE receptors, generation of intracellular signals, and histamine secretion in rat basophilic leukemia (2H3) cells. Enhanced responses with heavy water.

RBL-2H3 cells (a tumor analog of rat mast cells) have plasma-membrane receptors that bind immunoglobulin E, which when aggregated, initiate degranulation. As in other systems, secretion is preceeded by enhanced hydrolysis of inositol phospholipids and by a rise in intracellular Ca2+. Unlike the responses of many other cells, however, both of these earlier events require extracellular Ca2+. The relationship of these events to each other and to the subsequent secretory process is thus unclear. By exposing cells to covalent oligomers of IgE one can demonstrate substantial increases in secretion of histamine by increasing the concentration and size of the oligomers or by using heavy water (D2O) in the medium. We have used such maneuvers to examine the quantitative relationships between aggregation of the receptors and the breakdown of inositol phospholipids, the increase in cytosolic Ca2+ and secretion. Our principal findings were: all treatments that increased secretion, correspondingly increased the changes that precede degranulation. These early events correlated with the degree of aggregation of the receptors even when the stimulatory conditions resulted in maximal secretion. Although the results were insufficient to prove that the hydrolysis of inositol phospholipids is required for the rise in cytosolic Ca2+, the studies with D2O and other observations supported this view. Since a plasma-membrane ion channel for Ca2+ has been implicated in the IgE-mediated rise in cytosolic Ca2+ in RBL 2H3 cells, this in turn suggests a heretofore undescribed role for hydrolysis of inositol phospholipids.

Animals↗
PubMed1986

Immunohistochemical demonstration of histamine N-methyltransferase-like structures in rat kidney.

Histamine N-methyltransferase (S-adenosylmethionine: histamine N-methyltransferase, E.C. 2.1.1.8) was purified to homogeneity from rat kidney, and antibody was raised against it in guinea pigs. The antibody immunoprecipitated histamine N-methyltransferase. Immunofluorescent histochemical studies with anti-histamine N-methyltransferase antibody as the first antibody and goat anti-guinea pig IgG conjugated with fluorescein isothiocyanate as the second, showed the presence of immunoreactive structures in the proximal tubules of rat kidney. The brain showed no immunoreaction with the antibody.

Animals↗
PubMed1985

Effects of alpha-fluoromethylhistidine on sleep-waking parameters in rats.

Effects of alpha-fluoromethylhistidine (FMH), an irreversible inhibitor of histidine decarboxylase, on the sleep-waking parameters were studied in rats for 24 hours. Intraperitoneal administration of FMH (100 mg/kg) at 11:30 hr resulted in a longer sleep latency compared with the control values. Hour-to-hour analyses revealed that wakefulness (W) time decreased (from 20:00 to 07:00 hr) and slow wave sleep (SS) time increased (from 19:00 to 06:00 hr) in the night. Paradoxical sleep (PS) time did not parallel the SS changes; it was increased significantly from 07:00 to 11:00 hr in the next morning. The influence of FMH seemed to be divided into direct, immediate action (increase of W) and late, prolonged action (decrease of W), and the results obtained support the histamine arousal hypothesis.

Animals↗
PubMed1985

Non-IgG1 nature of cutaneous basophil hypersensitivity factor in contact sensitivity. III. Cutaneous basophil hypersensitivity factor promotes histamine release from guinea pig bone marrow basophils after antigenic stimulation.

Cutaneous basophil hypersensitivity factor (CBH-F) from the sera of 1-fluoro-2,4-dinitrobenzene contact-sensitized guinea pigs promoted histamine release from bone marrow basophils in the presence of the antigen, dinitrophenylated epidermal microsomes as well as in vivo activity to induce CBH reaction in naive recipients and in vitro activity to mediate antigen-dependent basophil chemotaxis. The amount of histamine released was around 20% of the total release when compared to that of concanavalin A-induced basophil degranulation (50-60%). Divalent cations were required in this reaction because addition of EDTA completely suppressed histamine release from passively sensitized basophils with CBH-F. Though it is not known at present whether the same molecule is involved in basophil chemotaxis and histamine release, this histamine-releasing activity was recovered in the same preparations with basophil chemotactic activity after several purification steps.

Animals↗
PubMed1985

Effects of alpha-fluoromethylhistidine on increase in histidine decarboxylase activity of maternal mouse kidney observed during late pregnancy and evidence for its non-mast cell origin by using estrogen and W/WV mice.

The increase of histidine decarboxylase (HDC) activity during late pregnancy in the whole bodies of fetal mice and the kidneys of their mothers were almost completely inhibited by i.p. administration of 25 mg/kg of alpha-fluoromethylhistidine (alpha-FMH), a suicide inhibitor of HDC, starting on day 13 of pregnancy. The increase of HDC in fetal mice was previously shown to be in mast cells [T. Watanabe et al., Proc. Natl. Acad. Sci. U.S.A. 78, 4209-4212 (1981)]. The increase of HDC in maternal kidneys was examined by using estrogen and W/WV mice, which were devoid of mast cells and infertile. Treatment of castrated mice with 17-beta-estradiol increased the HDC activity of the kidney, and this increase was antagonized by concomitant treatment with clomiphene, an antiestrogen, confirming that the increase is mediated through an estrogen receptor. HDC activity in the kidney of W/WV mice was also increased by estradiol treatment, indicating that HDC activity was associated with non-mast cells.

Animals↗
PubMed1984

The differential reaction of histamine and N tau-methylhistamine with Pauly's diazo reagent: application to assay of histamine N-methyltransferase activity.

A simple nonradioisotopic fluorescent method for assay of histamine N-methyltransferase (HMT) activity was developed. After termination of the HMT reaction, the remaining excess substrate, histamine, was degraded by Pauly 's diazo reagent, whereas the product, N tau-methylhistamine (N- MeHA ), was not degraded by the reagent. Then the mixture was applied to high-performance liquid chromatography under conditions in which N- MeHA was not separated from histamine, and N- MeHA was measured fluorometrically by condensation with o-phthalaldehyde. The method would be convenient for measurement of HMT activity during enzyme purification.

Animals↗
PubMed1984

Effect of food intake on urinary excretions of histamine, N tau-methylhistamine, imidazole acetic acid and its conjugate(s) in humans and mice.

The urinary excretions by young healthy men of histamine and its metabolites, N tau-methylhistamine, imidazole acetic acid, and imidazole acetic acid conjugate(s), increased 1-3 h after food intake. The increase was seen even after the intake of konnyaku (mannan) as a protein-deficient food, suggesting that physical stimulation of the gastric mucosa by food is the main cause of histamine release. This suggestion was confirmed by the following findings in patients and mice. In patients with stomach diseases, gastrectomy resulted in decreases in the excretion of histamine and its metabolites in the urine, and patients subjected to intravenous hyperalimentation excreted less histamine and its metabolites in the urine than normal subjects. In mice, a correlation of histamine excretion with food intake was demonstrated experimentally. Namely, mice fed only during the night (21:00-0:00) showed increased excretions of histamine and its metabolites at 23:00-3:00, whereas those fed in the morning (9:00-12:00) showed increased excretions of those compounds at 11:00-15:00. All these results are consistent with the idea that urinary histamine and its metabolites mainly originate from the stomach.

Adult↗
PubMed1984

Determination of imidazole acetic acid and its conjugate(s) levels in urine, serum and tissues of rats: studies on changes in their levels under various conditions.

A convenient and reproducible method for assay of imidazole acetic acid (ImAA) was developed as a modification of that described previously (Watanabe et al., 1983). ImAA conjugate(s) (ImAA-C), mainly consisting of imidazole acetic acid riboside, could be measured by this method after its hydrolysis to ImAA. The ImAA and ImAA-C levels in various tissues of rats were measured and the effects of various agents on these levels were studied. The renal clearance values of ImAA-C in rats and man were similar to the creatinine clearance values, but those of ImAA were 1/40 of those of ImAA-C, suggesting that the latter is readily excreted in the urine. Consistent with this idea, the urinary excretion of ImAA-C was found to increase much more than that of other histamine metabolites during late pregnancy, when the foetus produces much histamine.

Animals↗
PubMed1984

[Histamine].

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Animals↗
PubMed1983

Dopamine-producing endometrial carcinoma with argyrophilia.

A case of moderately differentiated adenocarcinoma with argyrophilia arising in the endometrium of a 58-year-old Japanese woman is reported. Although she showed no endocrine symptoms, neuro-secretory granules were documented in the cytoplasm of some tumor cells by electron microscopy. Moreover, dopamine production by the tumor was demonstrated by biochemical determination. The possible mechanism accounting for such a lesion is discussed.

Adenocarcinoma↗
PubMed1983

Effect of alpha-fluoromethylhistidine on the histamine content of the brain of W/Wv mice devoid of mast cells: turnover of brain histamine.

In the brains of W/Wv mutant mice that have no mast cells, the histidine decarboxylase (HDC) level is as high as in the brain of congenic normal mice (+/+), but the histamine content is 53% of that of +/+ mice. The effects of alpha-fluoromethylhistidine (alpha-FMH) on the HDC activity and histamine content of the brain of W/Wv and +/+ mice were examined. In both strains, 30 min after i.p. injection of alpha-FMH the HDC activity of the brain had decreased to 10% of that in untreated mice. The histamine content decreased more gradually, and after 6 h about half of the control level remained in +/+ mice, whereas histamine had disappeared almost completely in W/Wv mice. It is concluded that the portion of the histamine content that was depleted by HDC inhibitor in a short time is derived from non-mast cells, probably neural cells. The half-life of histamine in the brain of W/Wv mice was estimated from the time-dependent decrease in the histamine content of the brain after administration of alpha-FMH: 48 min in the forebrain, 103 min in the midbrain, and 66 min in the hindbrain.

Animals↗