共查询到20条相似文献,搜索用时 46 毫秒
1.
Dose dependent [14C]-histamine uptake is shown in ileal longitudinal muscle of the guinea pig in vitro; [14C]-radioactivity taken up is found only in part as unmodified histamine (7.9%) and for the remainder as histamine metabolites (N-methylhistamine 12.3% and acid metabolites 79.8%).This process is not affected by mast cell depletion obtained by means ofn-octylamine treatment.Theophylline and 3-isobutyl-1-methylxanthine (IMX) facilitate [14C]-histamine uptake, while -aminoguanidine inhibits it. Facilitation of histamine uptake by theophylline and IMX does not correlate with their ability to interfere with cAMP phosphodiesterase activity. While the first substance inhibits this activity, IMX, on the other hand, potentiates it.Variations of [14C]-histamine uptake parallel variations of [14C]-histamine metabolism: so an increase of [14C]-histamine uptake in the presence of theophylline or IMX is accompanied by an increase of acid metabolites, while in the presence of -aminoguanidine, which inhibits [14C]-histamine uptake, a decrease of acid metabolites is observed. The hypothesis is advanced that levels of unmodified histamine cause variations of negative feed-back on the transport system. 相似文献
2.
Objectives: Although the H4 receptor localisation in the eye is unresolved, this study aimed to investigate the effects of the H4 receptor antagonist JNJ7777120 in a model of experimental conjunctivitis.
Methods: JNJ7777120, at 0.005–1 mmol/l, was instilled into the lower conjunctival fornix of normal and compound 48/80 (C48/80)-challenged
eyes of male Wistar rats, in the absence or presence of 40 mg/ml disodium cromoglycate (DSCG). Conjunctival histamine content
was quantified 20 min post-challenge. Statistical analyses were performed by ANOVA.
Results: JNJ7777120 increased dose-dependently (r = 0.784, p < 0.001) the conjunctival histamine content. In the C48/80-challenged
eye no effect of the antagonist was observed. Co-administration of JNJ7777120 with DSCG resulted in a biphasic action of JNJ7777120,
implying a competitive action of the two agents.
Conclusions: These data suggest a functionality of the H4 receptor in the rat eye and address questions on the localization and the role of the receptor in ocular inflammation.
Received 15 October 2008; returned for revision 11 November 2008; received from final revision 18 November 2008; accepted
by A. Falus 22 November 2008 相似文献
3.
P. F. Mannaioni A. Pistelli M. G. Di Bello F. Gambassi E. Masini 《Inflammation research》1992,36(Z2):C402-C405
The influence of histamine on human platelet function was studied by measuring the uptake of [3H]-histamine and by evaluating the effect of histamine on Ca2+ influx and on intracellular Ca2+ levels. The uptake of histamine by platelets is significantly reduced by mepyramine and unaffected by cimetidine. Histamine was found to increase both the [45Ca]2+ uptake by resting and stimulated platelets, and the intracellular Ca2+ levels in Fura 2-AM loaded platelets. H1-antihistaminics significantly reduced these processes, suggesting a role for histamine, which in platelets promotes aggregation by acting through H1-receptors modulating intracellular Ca2+ levels. 相似文献
4.
Objective:Histamine stimulates nerve growth factor (NGF) secretion from cultured astrocytes. Histamine H1-receptor antagonists completely block its effect. In the present study, we determined the involvement of histamine-receptor subtypes in this process.Materials and methods:Radioligand-binding assay was used to establish the presence of histamine H1- and H2-receptors on new-born rat cortical astrocytes in primary culture. Histamine H1-, H2- and H3/H4-receptor ligands, and highly selective protein kinase C (PKC) inhibitor were used to influence NGF secretion from cultured astrocytes. NGF, released into the culture medium, was measured by NGF-ELISA.Results:Histamine H1-receptor agonists (histamine, selected histaprodifens) increased the secretion of NGF from cultured astrocytes in a concentration-dependent manner. H1-receptor antagonists/inverse agonists (mepyramine, triprolidine) and PKC inhibitor completely blocked the effect of histamine. Histamine H2- and H3-receptor agonists did not enhance NGF secretion significantly. In addition, H2- and H3/H4-receptor antagonists did not diminish histamine-stimulated NGF release.Conclusions:Our results indicate that histamine H1-receptor and PKC are involved in the signal transduction pathway, responsible for histamine-stimulated NGF secretion from cultured astrocytes.Received 25 July 2003; returned for revision 4 November 2003; accepted by A. Falus 23 December 2003 相似文献
5.
Objective and Design: To examine whether inhibitors of the MAPK pathways will influence the response of bovine chondrocytes cultured in agarose
constructs to IL-1β and dynamic compression.
Methods: Dose-response studies were conducted under IL-1β conditions with either SB203580, SP600125, PDTC or curcumin. In separate
experiments, constructs were treated with IL-1β and an appropriate concentration of inhibitor and subjected to 15% dynamic
compression. Nitrite and PGE2 release, 35SO4 and [3H]-thymidine incorporation were subsequently measured using biochemical assays.
Results: All inhibitors reduced the IL-1β induced nitrite and PGE2 release in a dose-dependent manner. The inhibition of [3H]-thymidine incorporation by IL-1β was partially reversed with SB203580, SP600125 or curcumin, but not PDTC. In most cases,
the inhibitors reduced 35SO4 incorporation with IL-1β. For the mechanical loading studies, the inhibitors reduced the compression-induced inhibition of
nitrite and PGE2 release and restored [3H]-thymidine and 35SO4 incorporation.
Conclusions: The MAPK, AP-1 and NF-κB signalling pathways are involved in the upregulation of NO and PGE2 release by IL-1β. Dynamic compression stimulates cell proliferation and proteoglycan synthesis in the presence of IL-1β and/or
inhibitors of the MAPKs and NFκB and AP-1 signalling pathways. This experimental approach could provide valuable information
for the biophysical/pharmacological treatment of OA.
Received 11 July 2007; returned for revision 27 September 2007; received from final revision 15 January 2008; accepted by
J. Di Battista 15 January 2008 相似文献
6.
Objective: In animal experiments many hormones were demonstrated in immune cells. However, very few data are at our disposal in the case
of human immune cells. In an earlier experiment, ACTH, endorphin and T3 were studied and found in different subsets of human immune cells. Here, three biogenic amines (histamine, serotonin and
epinephrine) were studied.
Methods: Biogenic amine content of immunophenotyped human lymphocytes from 15 blood donors were investigated by multicolor flow cytometry
using anti-biogenic amine antibodies. Monocytes and granulocytes separated by size and granularity were also studied.
Results: Each biogenic amine could be detected in each subset of leukocytes, except epinephrine and serotonin in granulocytes. Activated
T cells contained a higher amount of the amines, and CD19+B cells a higher amount of histamine, related to the whole lymphocyte
population and to other subsets. Monocytes contained more histamine and epinephrine than lymphocytes and granulocytes contained
twice as much histamine as monocytes and three times as much as lymphocytes.
Conclusion: Human lymphocytes contain the three biogenic amine, similar to rat. However, while each amine was present in monocytes, in
granulocytes serotonin and epinephrine were not demonstrated. The results call attention to the possible extrapolation of
animal data to human lymphocytes and monocytes, but in the case of granulocytes, caution is needed. Taking into consideration
earlier results, activated T cells appear to have an important role in the loss or production of hormones inside the immune
system.
Received 14 January 2008; returned for revision 11 February 2008; received from final revision 20 February 2008; accepted
by I. Ahnfelt-R?nne 18 March 2008 相似文献
7.
J. R. Aschenbach K. U. Honscha V. von Vietinghoff G. G?bel 《Inflammation research》2009,58(5):269-276
Objective: The study aimed to gain insight into how intestinal histamine N-methyltransferase (HMT) and diamine oxidase (DAO) could contribute
to bioelimination of histamine.
Material and Methods: Mucosal-to-serosal (ms) and serosal-to-mucosal (sm) fluxes of histamine, choline or 5-hydroxytryptamine were measured in isolated
colonic epithelia of pigs (Ussing chambers).
Results: Radioactively (hist-rad) and HPLC-measured histamine fluxes were higher in sm vs. ms direction at 100 μM histamine. Choline
(3–3000 μM) and 5-HT (20 μM) fluxes only tended to be higher in sm vs. ms direction. Secretion of hist-rad was abolished by
serosal 1-methyl-4-phenylpyridinium (MPP). Histamine fluxes accounted for <25 % of hist-rad fluxes, but this percentage increased
after blocking HMT (100 μM amodiaquin) or DAO (100 μM aminoguanidine). 1-Methylhistamine (1-MH) appeared exclusively in the
serosal medium. 1-MH appearance decreased after addition of amodiaquin or after addition of N-ethylmaleimide (1 mM NEM). Blockage
of vesicular trafficking by NEM enhanced histamine catabolism, which could be reversed by aminoguanidine. DAO was detected
in punctuate structures in the basal parts of colonocytes by immunohistochemistry.
Conclusions: A basolateral organic cation transporter facilitates histamine secretion into the intestinal lumen and delivers histamine
to catabolism by HMT and/or vesicular DAO. Histamine is partially released back into the blood after initial biotransformation
to 1-MH.
Received 7 May 2008; returned for revision 8 October 2008; received from final revision 2 November 2008; accepted by A. Falus
11 November 2008 相似文献
8.
Katsuhito Nagai Kazuki NagasawaRyoko Matsunaga Masumi YamajiSadaki Fujimoto 《Neuroscience letters》2006
Endogenous adenine is an important modulator of cell survival and activity in the central nervous system. In the present study, we examined the transport mechanisms for adenine in primary cultured rat cortical neurons and astrocytes. [3H]Adenine was time-dependently taken up into neurons, but not into astrocytes. In kinetic analysis, the [3H]adenine uptake by neurons was observed to be saturable, and an Eadie–Hofstee plot showed that a single component was involved in the uptake, with kinetic parameters of Km = 6.09 μM and Vmax = 0.340 nmol/mg protein per min. In inhibition assaying by nucleobases and nucleosides, and inhibitors for equilibrative nucleoside transporters, organic ion transporters and peptide transporters, which were reported to transport nucleobases and their analogues, the [3H]adenine uptake by neurons was found to be significantly inhibited by excess concentrations of adenine, hypoxanthine and adenosine, and was greatly reduced only by the addition of adenine. Therefore, it was indicated that adenine in the extracellular fluid in the central nervous system is taken up into neurons, but not into astrocytes, and that neurons may present a novel Na+-independent and adenine-specific transport system. 相似文献
9.
A. L. R. Barbosa C. A. Pinheiro G. J. Oliveira M. O. Moraes R. A. Ribeiro M. L. Vale M. H. L. P. Souza 《Inflammation research》2009,58(5):235-240
Objective and design: To investigate the effect of experimental tumor bearing on acute inflammation models in rats.
Methods: Four and 7 days after Walker tumor implantation in the right armpit, carrageenan or dextran– induced edema in the contralateral
paw, carrageenan induced neutrophil migration into peritoneal cavities, cutaneous vascular permeability induced by bradykinin,
histamine, serotonin, substance P, capsaicin or compound 48/80, and mesenteric mast cell degranulation induced by compound
48/80 were evaluated. The control group did not receive tumor implantation. Statistical analysis was performed using one way
analysis of variance (ANOVA) followed by the Bonferroni test.
Results: On the 7th day after tumor inoculation, there were significant decreases in both carrageenan and dextran- induced paw edema. Tumor bearing
did not change the neutrophil infiltration induced by carrageenan. There were decreases in cutaneous vascular permeability
induced by compound 48/80, serotonin or bradykinin, but not that induced by histamine, substance P. A significant inhibition
of mesenteric mast cell degranulation induced by compound 48/80 was observed, on the 4th and 7th days after tumor inoculation.
Conclusion: Tumor bearing can limit mast cell function and vascular events in acute systemic inflammation in rats, without changes in
neutrophil migration.
Received 20 July 2008; returned for revision 27 August 2008; received from final revision 4 November 2008; accepted by A.
Falus 6 November 2008 相似文献
10.
Sexual dimorphism has been demonstrated in rat brain and the ovarian steroids affect H1 and H2 histaminergic binding sites as demonstrated with [3H]-mepyramine and [3H]-histamine, respectively. The evaluation of histamine release, related to the presynaptic H3 receptors, from cortical slice preparations reveals hyposensitive releasing activity in the female rat compared to the male, both after KCl-induced histamine release and after inhibition of histamine release by (R)-methylhistamine (H3 selective agonist). Therefore, we may suggest a global hyposensitivity of the histaminergic neural system in female rats under the modulation of ovarian sexual steroids. 相似文献
11.
Background:Changes in the immune and inflammatory response are induced by smoking tobacco but underlying mechanisms remain to be elucidated.Objective:This study investigated the effect of nicotine agonists on histamine release from human basophils.Methods:Peripheral blood basophils were obtained from healthy volunteers. The effect of the nictotine agonists [–]-1-methyl-2-[3-pyridyl]pyrrolidine and (+)-nicotine di-p-toluoyltartrate salt on cell viability and anti-IgE induced histamine release was investigated.Results:Cell viability was not altered by preincubation with the agents for 15 min. Anti-IgE induced histamine release was significantly inhibited by preincubation (15 min, 37°C) with [–]-1-methyl-2-[3-pyridyl]pyrrolidine at the highest concentration tested 10–3 M (p<0.01). Preincubation (15 min, 37°C) with (+)-nicotine di-p-toluoyltartrate salt significantly inhibited anti-IgE induced histamine release at 10–3M and 10–5 M (p<0.05).Conclusions:This study has demonstrated that nicotine agonists inhibit histamine release from human basophils. Further studies examining the effect of smoking on basophil activation are required.Received 28 September 2003; returned for revision 1 December 2003; accepted by A. Falus 23 December 2003 相似文献
12.
Objective: To investigate the in vitro effects of H. pylori-conditioned medium (HCM) from gastric epithelial AGS cell cultures on microglia and neuronal cells.
Material: H. pylori, human gastric epithelial AGS cells, microglia-like BV-2 cells and human neuroblastoma SH-SY5Y cells.
Treatment: Treated AGS cells with H. pylori at ratios from 1:100 to 1:900 for 24 h. Cultured BV-2 cells and SH-SY5Y cells were treated with HCM from AGS cell cultures.
Methods: Cell viability was measured by a quantitative colorimetric assay with MTT. Nitric oxide (NO) was determined by using Griess
reagent. IL-8 was measured by an enzyme-linked immunosorbent assay. Protein expressions were revealed by western blot analysis.
Results: H. pylori increased IL-8, NO, COX-2 and gp91phox in AGS cell cultures. When BV-2 cells were cocultured with AGS cells, HCM increased COX-2, gp91phox, iNOS and NO of BV-2 cells. HCM also enhanced the degradation of IκBα in BV-2 cells. HCM up-regulated expression of nNOS,
COX-2, and gp91phox of SH-SY5Y cells co-cultured with BV-2 cells. Particularly, the decrease of cell viability of SH-SY5Y induced by HCM was
dependent on the presence of BV-2 cells.
Conclusions: H. pylori-induced infection induces microglia-mediated inflammation and neurotoxicity. The present results suggest that microglia play
a critical role in HCM-induced toxicity of neuronal SH-SY5Y cells.
Received 15 April 2008; returned for revision 10 May 2008; received from final revision 14 September 2008; accepted by M.
Katori 18 September 2008 相似文献
13.
S. Pierpaoli C. Marzocca M. G. Bello W. Schunack P. F. Mannaioni E. Masini 《Inflammation research》2003,52(9):390-396
Objective: The effects of histamine and of histamine receptor agonists and antagonists on the coronary outflow and on the generation of nitric oxide (NO) were evaluated on isolated guinea pig hearts.Methods: Isolated guinea pig hearts were perfused for 50 min in a Langendorff apparatus with histamine (10–7– 10–8 M), in the absence or in the presence of NG-monome-thyl-L-arginine (L-NMMA, 10–4 M), a NO synthase inhibitor and of triprolidine (310–8 M) and cimetidine (10–7 M), H1 receptor and H2 receptor antagonists, and with trifluoromethyl-phenylhistamine (TFMPH, 10–7 M) and dimaprit (10–7 M), H1 and H2 receptor agonists. The effects of (R)--methylhistamine (10–7 M), a H3 receptor agonist and of FUB 181 (10–7 M), a H3 receptor antagonist, were studied in the presence of bradykinin (10–7 M).Results: Histamine increases the coronary outflow and the generation of NO in a concentration-dependent fashion. The effects were completely abolished by blocking NO-synthase (NOS) with L-NMMA (10 –4 M). The effects were also abolished by cimetidine (10 –7 M), H 2 receptor antagonist, and only scarcely affected by triprolidine (310 –8 M), H 1 receptor antagonist. The effects were reproduced by dimaprit (10 –7 M), H 2 receptor agonist, and only scarcely by TFMPH (10 –7 M), a selective H 1 receptor agonist. Bradykinin (10 –7 M) produces a sustained coronary dilation paralleled by a marked increase in the generation of NO; the effects were significantly reduced by L-NMMA. The stimulation of H 3 receptors by (R)--methylhistamine (10 –7 M) significantly reduced both effects, which reverted to normal with FUB 181 (10 –7 M), an H 3 receptor antagonist.Conclusion: These results suggest that, in isolated guinea pig hearts, histamine produces coronary dilation through an H 2 /H 3 -dependent mechanism involving the generation of nitric oxide.Received 3 December 2002; returned for revision 8 April 2003; accepted by M. Parnham 26 May 2003 相似文献
14.
Objective: The objective was to investigate the role of histamine in the porcine caecum with special regard to its release and permeation.
Material and methods: Caecal epithelia were mounted in Ussing chambers. Mast cells were stimulated by A23187 (1 μmol/l). Permeation and changes
in short-circuit current (Isc) were assessed after unilateral application of 3H-labelled histamine (100 μmol/l). Mucosal-to-serosal (ms) and serosal- to-mucosal (sm) flux rates were calculated based on
the contralateral appearance of radioactive histamine label (hist-rad; representing histamine plus catabolites) as well as
histamine. 14C-mannitol fluxes were measured to assess paracellular permeability.
Results: Both A23187 and serosal addition of histamine increased Isc of caecal epithelia. The Isc increase due to A23187 was associated with an elevated histamine release from epithelia. A discrepancy between hist-rad and
histamine fluxes (P < 0.05) indicated effi cient histamine catabolism (ca. 85%), which was decreased by blockage of diamine
oxidase through aminoguanidine. Fluxes of histamine were correlated to 14C-mannitol fluxes. Fluxes of hist-rad and histamine were higher in the sm direction.
Conclusions: Histamine can be released from endogenous stores and acts on the epithelium. The absorption of luminal histamine is predominantly
restricted by paracellular permeability and catabolism. The latter is only partially catalysed by diamine oxidase.
Received 31 May 2005; returned for revision 11 August 2005; accepted by A. Falus 23 October 2005 相似文献
15.
N. Röver C. Krämer U. Stärk G. Gabriëls J. Greven 《Pflügers Archiv : European journal of physiology》1998,436(3):423-428
The kinetics of tubular glutarate uptake, the coupling of glutarate to p-aminohippurate (PAH) transport and the effect of activators of protein kinase A and C on glutarate uptake were studied using
isolated S2 segments of proximal tubules microdissected from rabbit kidneys without the use of enzymatic agents. Because the tubules
were not perfused, and hence were collapsed, the tubular uptake of [14C]glutarate reflects transport across the basolateral cell membrane. To obtain uptake rates most closely related to initial
transport rates, 30 s glutarate uptake measurements were performed. In a first set of experiments it could be shown that preloading
proximal S2 segments with glutarate (10–3 M) stimulated [3H]PAH uptake indicating that glutarate may be a substrate of the PAH /dicarboxylate exchanger. The kinetic data revealed a
K
m value of 0.62 mM and a V
max value of 84.1 pmol nl–1min–1 for tubular [14C]glutarate uptake across the basolateral cell membrane. In contrast to basolateral PAH transport (previous studies from this
laboratory), tubular 30 s [14C]glutarate uptake was not affected by either the phorbol ester phorbol 12-myristate 13-acetate (PMA, 10–7 M), an activator of protein kinase C, or by the membrane-permeant analogues of cAMP, dibutyryl cyclic AMP (db-cAMP, 10–4 M) and 8-bromoadenosine 3′,5′-cyclic monophosphate (Br-cAMP, 10–4 M). The results indicate that the protein kinases A and C have no function in the regulation of the renal basolateral dicarboxylate
transporter. This finding agrees well with the structural feature of the recently cloned rabbit renal dicarboxylate transporter
which does not contain any putative phosphorylation sites for protein kinase C or cAMP-dependent kinase.
Received: 30 December 1997 / Received after revision and accepted: 25 February 1998 相似文献
16.
Metabolic studies on the uptake of [14C]-histidine and [14C]-histamine and histamine synthesis by guinea-pig basophils, in vitro.
下载免费PDF全文
![点击此处可从《Immunology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
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. 相似文献
17.
In blood from the portal vein of anaesthetized rats the levels of histamine and putrescine were 2–3-fold lower compared to
arterial blood. Putrescine concentration was increased severalfold and the difference between portal and arterial blood abolished
in animals pretreated with the specific diamine oxidase inhibitor aminoguanidine. Histamine concentration was 40% lower in
portal compared to arterial blood in animals treated with the mast cell degranulator compound 48/80. In animals pretreated
with aminoguanidine, compound 48/80 enhanced the level of histamine and no difference was observed between arterial and portal
blood. The amounts of intravenously injected [14C]-labeled histamine was about 15% lower in portal compared to arterial blood. The uptake of [14C]-putrescine from the small intestine was estimated. In urine from animals pretreated with aminoguanidine the concentration
of [14C]-putrescine was more than 40-times higher than in control animals corresponding to a calculated uptake of about 7% in aminoguanidine
treated animals. Our results suggest that intestinal diamine oxidase clears the blood from diamines and prevents luminal uptake
of putrescine.
accepted by W. Lorenz 相似文献
18.
F. Martínez Martha Franco Alicia Quintana Jaime Herrera-Acosta 《Pflügers Archiv : European journal of physiology》1996,433(3):269-275
Studies of the uptake of [3H]adenosine ([3H]ADO) were performed using brush border membrane vesicles (BBMV) from normal (N) and hypothyroid (Tx) rat kidneys, to test
if decreased Na+ reabsorption in hypothyroidism might be associated with abnormalities in ADO transport. [3H]ADO uptake (1–10 μmol) for both conditions was measured in the presence of Na+ (10–150 mmol/l); the effects of dipyridamole (10 μmol/l) and 1,3-dipropyl-8-(2-amino-4-chlorophenyl)xanthine (PACPX, 10 μmol/l)
were also studied. Na+-stimulated ADO uptake was decreased in Tx BBMV. Michaelis–Menten constants showed a decreased ADO carrier affinity (K
m 2.46 ± 0.14 in N, vs K
m 4.46 ± 0.88 μmol/l in Tx, P<0.05), with no change in the number of carriers (V
max 295 ± 25 in N, vs 229.2 ± 56 pmol·min–1·mg protein in Tx). Na+ affinity remained unchanged (K
Na+ 11.5 ± 3.5 in N, vs K
Na+ 12.72 ± 0.7 mmol/l in Tx). Inhibition of Na+-dependent ADO transport was 50% in N as opposed to 58% in Tx with dipyridamole, and 72% in N versus 47% in Tx with PACPX.
These results suggest that decreased Na+-dependent ADO cotransport contributes to the diminished tubular reabsorption that occurs in hypothyroidism.
Received: 17 June 1996 / Received after revision: 9 September 1996 / Accepted: 16 September 1996 相似文献
19.
Christian Gespach Jean-Marie Launay Shahin Emami Dominique Bondoux Claude Dreux 《Inflammation research》1986,18(1-2):115-119
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 2.5×10–7 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 mimiked 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>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 receptors antagonists (H2h), mediating 5-HT uptake in human platelets. 相似文献
20.
Objective and design:The roles of histamine formed by the macrophage – T lymphocyte system were evaluated in the regulation of lymphocyte proliferation using mice lacking histamine receptors.
Methods:Mice deficient in histamine type 1 (H1R), type 2 (H2R) or both receptors were employed to estimate possible intervention of the receptors in the histamine-dependent lymphocyte proliferation.
Results:Histamine was produced de novo by spleen cells. Con A-dependent T cell proliferation decreased when histamine produced in the culture was degraded by the addition of histaminase. The H2R-deficient mice also showed a significant decrease in the Con A-dependent T cell proliferation, whereas it was not modulated in the H1R-deleted mice. Consistent with the reduction in T cell proliferation, there was a significant down-regulation of the production of IL-2, a T cell growth factor, in the H2R-deficient mice. Con A-dependent IL-2 synthesis was abrogated by the addition of histaminase.
Conclusions:Con A-dependent T cell proliferation is (up)regulated by histamine produced de novo through the H2R, suggesting that histamine is a newly found regulator of T cell proliferation.Received 18 October 2003; returned for revision 17 December 2003; accepted by M. J. Parnham 6 February 2004 相似文献