Base de dados : MEDLINE
Pesquisa : D12.776.543.750.670.450.300 [Categoria DeCS]
Referências encontradas : 2152 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 216 ir para página                         

  1 / 2152 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29239411
[Au] Autor:Ogasawara H; Grzybowski M; Hosokawa R; Sato Y; Taki M; Yamaguchi S
[Ad] Endereço:Department of Chemistry, Graduate School of Science and Integrated Research Consortium on Chemical Sciences (IRCCS), Nagoya University, Furo, Chikusa, Nagoya 464-8602, Japan.
[Ti] Título:A far-red fluorescent probe based on a phospha-fluorescein scaffold for cytosolic calcium imaging.
[So] Source:Chem Commun (Camb);54(3):299-302, 2018 Jan 02.
[Is] ISSN:1364-548X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The far-red emissive fluorescent probe CaPF-1 based on a phospha-fluorescein scaffold enables the detection of cytosolic calcium ions in living cells. The probe can be excited in the red region (λ = 636 nm) and exhibits a sufficiently high fluorescence turn-on response in the far-red region (λ = 663 nm) upon complexation with calcium ions. The hydrophilic and anionic characteristics of this phospha-fluorescein fluorophore allowed the cytosolic localization of CaPF-1. Moreover, it was possible to visualize histamine-induced calcium oscillation in HeLa cells using CaPF-1.
[Mh] Termos MeSH primário: Cálcio/análise
Óxidos P-Cíclicos/farmacologia
Fluoresceínas/farmacologia
Corantes Fluorescentes/farmacologia
[Mh] Termos MeSH secundário: Cálcio/metabolismo
Óxidos P-Cíclicos/síntese química
Óxidos P-Cíclicos/química
Fluoresceínas/síntese química
Fluoresceínas/química
Fluorescência
Corantes Fluorescentes/síntese química
Corantes Fluorescentes/química
Células HeLa
Histamina/metabolismo
Seres Humanos
Concentração de Íons de Hidrogênio
Microscopia Confocal
Imagem Molecular
Imagem Óptica
Receptores Histamínicos H1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cyclic P-Oxides); 0 (Fluoresceins); 0 (Fluorescent Dyes); 0 (Receptors, Histamine H1); 820484N8I3 (Histamine); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1039/c7cc07344e


  2 / 2152 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28939039
[Au] Autor:Wang B; An N; Shaikh AS; Wang H; Xiao L; Liu H; Li J; Zhao D
[Ad] Endereço:Department of Physiology, Shandong Provincial Key Laboratory of Mental Disorders, Shandong University School of Medicine, Jinan, China.
[Ti] Título:Hyperosmolarity evokes histamine release from ileum mucosa by stimulating a cholinergic pathway.
[So] Source:Biochem Biophys Res Commun;493(2):1037-1042, 2017 Nov 18.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Changes in extracellular osmolarity lead to alteration in cellular volume. In the study, we examined the effects of hyperosmolarity on short-circuit currents (Isc) in the rat ileum using the Ussing chamber technique. Mucosal exposure to 20 mM glucose evoked a decrease of I in the rat ileum, which was antagonized by the stretch-activated channel blocker GdCl3, TTX and atropine, respectively. In contrast, it was not blocked by phlorizin, a Na -glucose cotransporter SGLT1 inhibitor. Furthermore, the unabsorbed substances, such as sucrose, lactulose or urea, also induced a decrease of I in rat ileum. ELISA results revealed that 20 mM glucose stimulated the release of histamine from rat ileum mucosa, which was attenuated by TTX. In addition, the glucose-induced I was depressed by pyrilamine, a histamine H receptor blocker (H antagonist) whereas it was not affected by ranitidine (H antagonist), clobenpropit (H antagonists) or JNJ7777120 (H antagonist), respectively. The ion substitution experiments suggest that the changes of Na and HCO ion flux underlie the glucose-induced I In conclusion, osmotic stimulus decreased the basal I of rat ileum by evoking histamine release from ileum mucosa. The changes of Na and HCO ion transport are involved in the glucose-evoked decrease of basal I .
[Mh] Termos MeSH primário: Liberação de Histamina
Íleo/fisiologia
Mucosa Intestinal/fisiologia
Pressão Osmótica
[Mh] Termos MeSH secundário: Animais
Bicarbonatos/metabolismo
Tamanho Celular/efeitos dos fármacos
Glucose/metabolismo
Histamina/metabolismo
Antagonistas dos Receptores Histamínicos/farmacologia
Liberação de Histamina/efeitos dos fármacos
Íleo/citologia
Íleo/efeitos dos fármacos
Mucosa Intestinal/efeitos dos fármacos
Transporte de Íons/efeitos dos fármacos
Masculino
Concentração Osmolar
Ratos
Ratos Wistar
Receptores Histamínicos H1/metabolismo
Sódio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Bicarbonates); 0 (Histamine Antagonists); 0 (Receptors, Histamine H1); 820484N8I3 (Histamine); 9NEZ333N27 (Sodium); IY9XDZ35W2 (Glucose)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170924
[St] Status:MEDLINE


  3 / 2152 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28797771
[Au] Autor:Lazewska D; Kaleta M; Schwed JS; Karcz T; Mogilski S; Latacz G; Olejarz A; Siwek A; Kubacka M; Lubelska A; Honkisz E; Handzlik J; Filipek B; Stark H; Kiec-Kononowicz K
[Ad] Endereço:Department of Technology and Biotechnology of Drugs, Faculty of Pharmacy, Jagiellonian University Medical College, ul. Medyczna 9, 30-688 Kraków, Poland. Electronic address: dlazewska@cm-uj.krakow.pl.
[Ti] Título:Biphenyloxy-alkyl-piperidine and azepane derivatives as histamine H receptor ligands.
[So] Source:Bioorg Med Chem;25(20):5341-5354, 2017 Oct 15.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Novel biphenyloxy-alkyl derivatives of piperidine and azepane were synthesized and evaluated for their binding properties at the human histamine H receptor. Two series of compounds were obtained with a meta- and a para-biphenyl moiety. The alkyl chain spacer contained five and six carbon atoms. The highest affinity among all compounds was shown by 1-(6-(3-phenylphenoxy)hexyl)azepane (13) with a K value of 18nM. Two para-biphenyl derivatives, 1-(5-(4-phenylphenoxy)pentyl)piperidine (14; K =25nM) and 1-(5-(4-phenylphenoxy)pentyl)azepane (16; K =34nM), classified as antagonists in a cAMP accumulation assay (IC =4 and 9nM, respectively), were studied in detail. Compounds 14 and 16 blocked RAMH-induced dipsogenia in rats (ED of 2.72mg/kg and 1.75mg/kg respectively), and showed high selectivity (hH R vs hH R>600-fold) and low toxicity (hERG inhibition: IC >1.70µM; hepatotoxicity IC >12.5µM; non-mutagenic up to 10µM). Furthermore, the metabolic stability was evaluated in vitro on human liver microsomes (HLMs) and/or rat liver microsomes (RLMs). Metabolites produced were analyzed and tentatively identified by UPLC-MS techniques. The results demonstrated easy hydroxylation of the biphenyl ring.
[Mh] Termos MeSH primário: Azepinas/farmacologia
Piperidinas/farmacologia
Receptores Histamínicos H3/metabolismo
[Mh] Termos MeSH secundário: Animais
Azepinas/síntese química
Azepinas/química
Proliferação Celular
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Cobaias
Células HEK293
Células Hep G2
Seres Humanos
Ligantes
Masculino
Estrutura Molecular
Piperidinas/síntese química
Piperidinas/química
Ratos
Ratos Wistar
Receptor Muscarínico M3/antagonistas & inibidores
Receptor Muscarínico M3/metabolismo
Receptores Histamínicos H1/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Azepines); 0 (Ligands); 0 (Piperidines); 0 (Receptor, Muscarinic M3); 0 (Receptors, Histamine H1); 0 (Receptors, Histamine H3); 67I85E138Y (piperidine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170812
[St] Status:MEDLINE


  4 / 2152 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28275716
[Au] Autor:Chen A; Singh C; Oikonomou G; Prober DA
[Ad] Endereço:Division of Biology and Biological Engineering, California Institute of Technology , Pasadena, CA 91125.
[Ti] Título:Genetic Analysis of Histamine Signaling in Larval Zebrafish Sleep.
[So] Source:eNeuro;4(1), 2017 Jan-Feb.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Pharmacological studies in mammals and zebrafish suggest that histamine plays an important role in promoting arousal. However, genetic studies using rodents with disrupted histamine synthesis or signaling have revealed only subtle or no sleep/wake phenotypes. Studies of histamine function in mammalian arousal are complicated by its production in cells of the immune system and its roles in humoral and cellular immunity, which can have profound effects on sleep/wake states. To avoid this potential confound, we used genetics to explore the role of histamine in regulating sleep in zebrafish, a diurnal vertebrate in which histamine production is restricted to neurons in the brain. Similar to rodent genetic studies, we found that zebrafish that lack histamine due to mutation of histidine decarboxylase ( ) exhibit largely normal sleep/wake behaviors. Zebrafish containing predicted null mutations in several histamine receptors also lack robust sleep/wake phenotypes, although we are unable to verify that these mutants are completely nonfunctional. Consistent with some rodent studies, we found that arousal induced by overexpression of the neuropeptide hypocretin (Hcrt) or by stimulation of -expressing neurons is not blocked in or mutants. We also found that the number of -expressing or histaminergic neurons is unaffected in animals that lack histamine or Hcrt signaling, respectively. Thus, while acute pharmacological manipulation of histamine signaling has been shown to have profound effects on zebrafish and mammalian sleep, our results suggest that chronic loss of histamine signaling due to genetic mutations has only subtle effects on sleep in zebrafish, similar to rodents.
[Mh] Termos MeSH primário: Histamina/genética
Histamina/metabolismo
Receptores Histamínicos H1/genética
Receptores Histamínicos H1/metabolismo
Sono/genética
Sono/fisiologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Ensaio de Imunoadsorção Enzimática
Histidina Descarboxilase/deficiência
Histidina Descarboxilase/genética
Imuno-Histoquímica
Larva
Neurônios/citologia
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
Optogenética
Orexinas/genética
Orexinas/metabolismo
Estimulação Física
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Vigília/fisiologia
Peixe-Zebra
Proteínas de Peixe-Zebra/genética
Proteínas de Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hcrt protein, zebrafish); 0 (Orexins); 0 (Receptors, Histamine H1); 0 (Zebrafish Proteins); 820484N8I3 (Histamine); EC 4.1.1.22 (Histidine Decarboxylase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE


  5 / 2152 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28190755
[Au] Autor:Kanamitsu K; Nozaki Y; Nagaya Y; Sugiyama Y; Kusuhara H
[Ad] Endereço:Laboratory of Molecular Pharmacokinetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan; Tokushima Research Institute, Otsuka Pharmaceutical Co., Ltd., 463-10 Kagasuno, Kawauchi-cho, Tokushima-shi, Tokushima, 771-0192, Japan.
[Ti] Título:Quantitative prediction of histamine H1 receptor occupancy by the sedative and non-sedative antagonists in the human central nervous system based on systemic exposure and preclinical data.
[So] Source:Drug Metab Pharmacokinet;32(2):135-144, 2017 Apr.
[Is] ISSN:1880-0920
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Significant histamine H1 receptor occupation in the central nervous system (CNS) is associated with sedation. Here we examined the time profiles of the H1 receptor occupancy (RO) in the CNS using sedative (diphenhydramine and ketotifen) and non-sedative (bepotastine and olopatadine) antagonists at their therapeutic doses by integrating in vitro and animal data. A pharmacokinetic model was constructed to associate plasma concentrations and receptor binding in the brain. Dissociation and association rate constants with the H1 receptor and plasma and brain unbound fractions were determined in vitro. Passive and active clearances across the blood-brain barrier (BBB) were estimated based on physicochemical properties and microdialysis studies in mice and monkeys. The estimated RO values were comparable with the reported values determined at time to maximum concentration (T ) of plasma by positron-emission tomography in humans. The simulation suggested that the predicted maximum ROs by bepotastine and olopatadine were greater than the reported values. Sensitivity analysis showed that active transport across BBB had a significant impact on the RO duration of the H1 antagonists examined. The present study demonstrated that modeling and simulation permits a reasonable RO estimation in the human CNS. Our findings will facilitate the development of CNS-acting drugs.
[Mh] Termos MeSH primário: Sistema Nervoso Central/efeitos dos fármacos
Antagonistas dos Receptores Histamínicos H1/farmacologia
Receptores Histamínicos H1/metabolismo
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Sistema Nervoso Central/metabolismo
Difenidramina/sangue
Difenidramina/farmacologia
Antagonistas dos Receptores Histamínicos H1/sangue
Seres Humanos
Cetotifeno/sangue
Cetotifeno/farmacologia
Macaca fascicularis
Masculino
Camundongos
Camundongos Endogâmicos
Cloridrato de Olopatadina/sangue
Cloridrato de Olopatadina/farmacologia
Piperidinas/sangue
Piperidinas/farmacologia
Tomografia por Emissão de Pósitrons
Piridinas/sangue
Piridinas/farmacologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histamine H1 Antagonists); 0 (Piperidines); 0 (Pyridines); 0 (Receptors, Histamine H1); 2XG66W44KF (Olopatadine Hydrochloride); 8GTS82S83M (Diphenhydramine); HYD2U48IAS (bepotastine); X49220T18G (Ketotifen)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170505
[Lr] Data última revisão:
170505
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170214
[St] Status:MEDLINE


  6 / 2152 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28188663
[Au] Autor:Cilz NI; Lei S
[Ad] Endereço:Department of Biomedical Sciences, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, North Dakota.
[Ti] Título:Histamine facilitates GABAergic transmission in the rat entorhinal cortex: Roles of H and H receptors, Na -permeable cation channels, and inward rectifier K channels.
[So] Source:Hippocampus;27(5):613-631, 2017 May.
[Is] ISSN:1098-1063
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the brain, histamine (HA) serves as a neuromodulator and a neurotransmitter released from the tuberomammillary nucleus (TMN). HA is involved in wakefulness, thermoregulation, energy homeostasis, nociception, and learning and memory. The medial entorhinal cortex (MEC) receives inputs from the TMN and expresses HA receptors (H , H , and H ). We investigated the effects of HA on GABAergic transmission in the MEC and found that HA significantly increased the frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) with an EC of 1.3 µM, but failed to significantly alter sIPSC amplitude. HA-induced increases in sIPSC frequency were sensitive to tetrodotoxin (TTX), required extracellular Ca , and persisted when GDP-ß-S, a G-protein inactivator, was applied postsynaptically via the recording pipettes, indicating that HA increased GABA release by facilitating the excitability of GABAergic interneurons in the MEC. Recordings from local MEC interneurons revealed that HA significantly increased their excitability as determined by membrane depolarization, generation of an inward current at -65 mV, and augmentation of action potential firing frequency. Both H and H receptors were involved in HA-induced increases in sIPSCs and interneuron excitability. Immunohistochemical staining showed that both H and H receptors are expressed on GABAergic interneurons in the MEC. HA-induced depolarization of interneurons involved a mixed ionic mechanism including activation of a Na -permeable cation channel and inhibition of a cesium-sensitive inward rectifier K channel, although HA also inhibited the delayed rectifier K channels. Our results may provide a cellular mechanism, at least partially, to explain the roles of HA in the brain. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Córtex Entorrinal/metabolismo
Histamina/metabolismo
Interneurônios/metabolismo
Transmissão Sináptica/fisiologia
Ácido gama-Aminobutírico/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/fisiologia
Animais
Cálcio/metabolismo
Cátions/metabolismo
Césio/metabolismo
Córtex Entorrinal/citologia
Córtex Entorrinal/efeitos dos fármacos
Agonistas dos Receptores Histamínicos/farmacologia
Antagonistas dos Receptores Histamínicos/farmacologia
Interneurônios/citologia
Interneurônios/efeitos dos fármacos
Canais de Potássio Corretores do Fluxo de Internalização/metabolismo
Ratos Sprague-Dawley
Receptores de GABA-A/metabolismo
Receptores Histamínicos H1/metabolismo
Receptores Histamínicos H2/metabolismo
Receptores Histamínicos H3/metabolismo
Bloqueadores dos Canais de Sódio/farmacologia
Canais de Sódio/metabolismo
Transmissão Sináptica/efeitos dos fármacos
Técnicas de Cultura de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cations); 0 (Histamine Agonists); 0 (Histamine Antagonists); 0 (Potassium Channels, Inwardly Rectifying); 0 (Receptors, GABA-A); 0 (Receptors, Histamine H1); 0 (Receptors, Histamine H2); 0 (Receptors, Histamine H3); 0 (Sodium Channel Blockers); 0 (Sodium Channels); 1KSV9V4Y4I (Cesium); 56-12-2 (gamma-Aminobutyric Acid); 820484N8I3 (Histamine); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170425
[Lr] Data última revisão:
170425
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170212
[St] Status:MEDLINE
[do] DOI:10.1002/hipo.22718


  7 / 2152 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28178593
[Au] Autor:Wolak M; Bojanowska E; Staszewska T; Ciosek J; Juszczak M; Drobnik J
[Ad] Endereço:Department of Behavioral Pathophysiology, Chair of General and Experimental Pathology Medical University of Lodz, Lódz, Poland.
[Ti] Título:The role of histamine in the regulation of the viability, proliferation and transforming growth factor ß1 secretion of rat wound fibroblasts.
[So] Source:Pharmacol Rep;69(2):314-321, 2017 Apr.
[Is] ISSN:1734-1140
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Inflammation mediators play a regulatory role in repair processes. The study will examine the influence of histamine on wound fibroblast metabolic activity, viability, proliferation, and TGFß1 secretion. The study also will identify the histamine receptor involved in regulation of the tested repair processes. METHODS: Fibroblasts were obtained from the granulation tissue of wounds or intact dermis of rats. The MTT and BrdU assays were used to examine the effect of histamine (10 M-10 M) on the viability and metabolic activity of fibroblasts, and on their proliferative capacity. The influence of histamine receptor antagonists (i.e., ketotifen, ranitidine, ciproxifan and JNJ7777120) and agonists (2-pyridylethlamine dihydrochloride, amthamine dihydrobromide) was also investigated. The TGFß1 and histamine receptors H1 were evaluated by enzyme-linked immunosorbent assay. RESULTS: Histamine significantly increased granulation tissue fibroblast viability and metabolic activity at 10 and 10 M but did not change their proliferative activity. Only the blockade of the H1 receptor removed this effect of histamine. H1 receptor agonist (2-pyridylethlamine dihydrochloride) increased cell viability, thereby mimicking histamine action. Both Histamine (10 M) and 2-pyridylethlamine dihydrochloride increased TGFß1 concentration in cell culture medium. However, ketotifen blocked histamine-induced augmentation of TGFß1. H1 receptor expression on wound fibroblasts was confirmed. CONCLUSION: The regulatory influence of histamine on wound fibroblast function (viability/metabolic activity or secretion of TGFß1) is dependent on H1 receptor stimulation. Contrary to wound fibroblasts, these cells express a very low level of H1 receptors when isolated from intact dermis and histamine is unable to modify their metabolic activity.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Fibroblastos/efeitos dos fármacos
Histamina/farmacologia
Fator de Crescimento Transformador beta1/metabolismo
Cicatrização/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Fibroblastos/metabolismo
Agonistas dos Receptores Histamínicos/farmacologia
Antagonistas dos Receptores Histamínicos H1/farmacologia
Masculino
Ratos
Ratos Wistar
Receptores Histamínicos H1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histamine Agonists); 0 (Histamine H1 Antagonists); 0 (Receptors, Histamine H1); 0 (Transforming Growth Factor beta1); 820484N8I3 (Histamine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170323
[Lr] Data última revisão:
170323
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE


  8 / 2152 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28040476
[Au] Autor:Hishinuma S; Kosaka K; Akatsu C; Uesawa Y; Fukui H; Shoji M
[Ad] Endereço:Department of Pharmacodynamics, Meiji Pharmaceutical University, 2-522-1 Noshio, Kiyose, Tokyo 204-8588, Japan. Electronic address: hishi@my-pharm.ac.jp.
[Ti] Título:Asp73-dependent and -independent regulation of the affinity of ligands for human histamine H receptors by Na .
[So] Source:Biochem Pharmacol;128:46-54, 2017 Mar 15.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The affinity of ligands for G-protein-coupled receptors (GPCRs) is allosterically regulated by Na via a highly conserved aspartate residue (Asp ) in the second transmembrane domain of GPCRs. In the present study, we examined the Na -mediated regulation of the affinity of ligands for G -protein-coupled human histamine H receptors in Chinese hamster ovary cells. The affinities of 3 agonists and 20 antihistamines were evaluated by their displacement curves against the binding of [ H]-mepyramine to membrane preparations in the presence or absence of 100mM NaCl. The affinities of most drugs including histamine, an agonist, and d-chlorpheniramine, a first-generation antihistamine, were reduced by NaCl, with the extent of NaCl-mediated changes varying widely between drugs. In contrast, the affinities of some second-generation antihistamines such as fexofenadine were increased by NaCl. These changes were retained in intact cells. The mutation of Asp (Asp73) to asparagine abrogated NaCl-induced reductions in affinities for histamine and d-chlorpheniramine, but not NaCl-induced increases in the affinity for fexofenadine. Quantitative structure-activity relationship (QSAR) analyses showed that these Na -mediated changes were explained and predicted by a combination of the molecular energies and implicit solvation energies of the compounds. These results suggest that Na diversely regulates the affinity of ligands for H receptors from the extracellular sites of receptors via Asp73-dependent and -independent mechanisms in a manner that depends on the physicochemical properties of ligands. These results may contribute to a deeper understanding of the fundamental mechanisms by which the affinity of ligands for their receptors is allosterically regulated by Na .
[Mh] Termos MeSH primário: Ácido Aspártico/genética
Receptores Histamínicos H1/fisiologia
Cloreto de Sódio/farmacologia
[Mh] Termos MeSH secundário: Animais
Células CHO
Cátions Monovalentes
Clorfeniramina/farmacologia
Cricetulus
Histamina/farmacologia
Agonistas dos Receptores Histamínicos/farmacologia
Antagonistas dos Receptores Histamínicos H1/farmacologia
Seres Humanos
Ligantes
Mutação
Relação Quantitativa Estrutura-Atividade
Ensaio Radioligante
Receptores Histamínicos H1/genética
Terfenadina/análogos & derivados
Terfenadina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cations, Monovalent); 0 (Histamine Agonists); 0 (Histamine H1 Antagonists); 0 (Ligands); 0 (Receptors, Histamine H1); 30KYC7MIAI (Aspartic Acid); 3U6IO1965U (Chlorpheniramine); 451W47IQ8X (Sodium Chloride); 7BA5G9Y06Q (Terfenadine); 820484N8I3 (Histamine); E6582LOH6V (fexofenadine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170102
[St] Status:MEDLINE


  9 / 2152 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27914963
[Au] Autor:Carlin JL; Jain S; Gizewski E; Wan TC; Tosh DK; Xiao C; Auchampach JA; Jacobson KA; Gavrilova O; Reitman ML
[Ad] Endereço:Diabetes, Endocrinology, and Obesity Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA.
[Ti] Título:Hypothermia in mouse is caused by adenosine A and A receptor agonists and AMP via three distinct mechanisms.
[So] Source:Neuropharmacology;114:101-113, 2017 Mar 01.
[Is] ISSN:1873-7064
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Small mammals have the ability to enter torpor, a hypothermic, hypometabolic state, allowing impressive energy conservation. Administration of adenosine or adenosine 5'-monophosphate (AMP) can trigger a hypothermic, torpor-like state. We investigated the mechanisms for hypothermia using telemetric monitoring of body temperature in wild type and receptor knock out (Adora1 , Adora3 ) mice. Confirming prior data, stimulation of the A adenosine receptor (AR) induced hypothermia via peripheral mast cell degranulation, histamine release, and activation of central histamine H receptors. In contrast, A AR agonists and AMP both acted centrally to cause hypothermia. Commonly used, selective A AR agonists, including N -cyclopentyladenosine (CPA), N -cyclohexyladenosine (CHA), and MRS5474, caused hypothermia via both A AR and A AR when given intraperitoneally. Intracerebroventricular dosing, low peripheral doses of Cl-ENBA [(±)-5'-chloro-5'-deoxy-N -endo-norbornyladenosine], or using Adora3 mice allowed selective stimulation of A AR. AMP-stimulated hypothermia can occur independently of A AR, A AR, and mast cells. A AR and A AR agonists and AMP cause regulated hypothermia that was characterized by a drop in total energy expenditure, physical inactivity, and preference for cooler environmental temperatures, indicating a reduced body temperature set point. Neither A AR nor A AR was required for fasting-induced torpor. A AR and A AR agonists and AMP trigger regulated hypothermia via three distinct mechanisms.
[Mh] Termos MeSH primário: Agonistas do Receptor A1 de Adenosina/administração & dosagem
Agonistas do Receptor A3 de Adenosina/administração & dosagem
Monofosfato de Adenosina/fisiologia
Febre/induzido quimicamente
Receptor A1 de Adenosina/fisiologia
Receptor A3 de Adenosina/fisiologia
Torpor
[Mh] Termos MeSH secundário: Adenosina/administração & dosagem
Adenosina/análogos & derivados
Animais
Encéfalo/efeitos dos fármacos
Encéfalo/fisiologia
Histamina/metabolismo
Injeções Intraventriculares
Masculino
Mastócitos/efeitos dos fármacos
Mastócitos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Receptor A1 de Adenosina/genética
Receptor A3 de Adenosina/genética
Receptores Histamínicos H1/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adenosine A1 Receptor Agonists); 0 (Adenosine A3 Receptor Agonists); 0 (Receptor, Adenosine A1); 0 (Receptor, Adenosine A3); 0 (Receptors, Histamine H1); 36396-99-3 (N(6)-cyclohexyladenosine); 41552-82-3 (N(6)-cyclopentyladenosine); 415SHH325A (Adenosine Monophosphate); 820484N8I3 (Histamine); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161205
[St] Status:MEDLINE


  10 / 2152 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27904941
[Au] Autor:Fischer L; Lavoranti MI; de Oliveira Borges M; Miksza AF; Sardi NF; Martynhak BJ; Tambeli CH; Parada CA
[Ad] Endereço:Division of Biological Sciences, Department of Physiology, Federal University of Parana, Curitiba, Parana, Brazil. fischer@ufpr.br.
[Ti] Título:TRPA1, substance P, histamine and 5-hydroxytryptamine interact in an interdependent way to induce nociception.
[So] Source:Inflamm Res;66(4):311-322, 2017 Apr.
[Is] ISSN:1420-908X
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Although TRPA1, SP, histamine and 5-hydroxytryptamine (5-HT) have recognized contribution to nociceptive mechanisms, little is known about how they interact with each other to mediate inflammatory pain in vivo. In this study we evaluated whether TRPA1, SP, histamine and 5-HT interact, in an interdependent way, to induce nociception in vivo. METHODS AND RESULTS: The subcutaneous injection of the TRPA1 agonist allyl isothiocyanate (AITC) into the rat's hind paw induced a dose-dependent and short lasting behavioral nociceptive response that was blocked by the co-administration of the TRPA1 antagonist, HC030031, or by the pretreatment with antisense ODN against TRPA1. AITC-induced nociception was significantly decreased by the co-administration of selective antagonists for the NK1 receptor for substance P, the H1 receptor for histamine and the 5-HT receptors for 5-HT. Histamine- or 5-HT-induced nociception was decreased by the pretreatment with antisense ODN against TRPA1. These findings suggest that AITC-induced nociception depends on substance P, histamine and 5-HT, while histamine- or 5-HT-induced nociception depends on TRPA1. Most important, AITC interact in a synergistic way with histamine, 5-HT or substance P, since their combination at non-nociceptive doses induced a nociceptive response much higher than that expected by the sum of the effect of each one alone. This synergistic effect is dependent on the H1, 5-HT receptors. CONCLUSION: Together, these findings suggest a self-sustainable cycle around TRPA1, no matter where the cycle is initiated each step is achieved and even subeffective activation of more than one step results in a synergistic activation of the overall cycle.
[Mh] Termos MeSH primário: Histamina/metabolismo
Dor/metabolismo
Serotonina/metabolismo
Substância P/metabolismo
Canais de Cátion TRPC/metabolismo
[Mh] Termos MeSH secundário: Acetanilidas/farmacologia
Animais
Antagonistas dos Receptores Histamínicos H1/farmacologia
Isotiocianatos
Masculino
Oligonucleotídeos Antissenso/farmacologia
Dor/induzido quimicamente
Piperazinas/farmacologia
Purinas/farmacologia
Pirilamina/farmacologia
Quinuclidinas/farmacologia
Ratos Wistar
Receptor 5-HT1A de Serotonina/metabolismo
Receptores Histamínicos H1/metabolismo
Receptores da Neurocinina-1/metabolismo
Receptores 5-HT3 de Serotonina/metabolismo
Antagonistas da Serotonina/farmacologia
Canal de Cátion TRPA1
Canais de Cátion TRPC/agonistas
Canais de Cátion TRPC/antagonistas & inibidores
Canais de Cátion TRPC/genética
p-Metoxi-N-metilfenetilamina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (2-(1,3-dimethyl-2,6-dioxo-1,2,3,6-tetrahydro-7H-purin-7-yl)-N-(4-isopropylphenyl)acetamide); 0 (Acetanilides); 0 (Histamine H1 Antagonists); 0 (Isothiocyanates); 0 (Oligonucleotides, Antisense); 0 (Piperazines); 0 (Purines); 0 (Quinuclidines); 0 (Receptors, Histamine H1); 0 (Receptors, Neurokinin-1); 0 (Receptors, Serotonin, 5-HT3); 0 (Serotonin Antagonists); 0 (TRPA1 Cation Channel); 0 (TRPC Cation Channels); 0 (Trpa1 protein, rat); 112692-38-3 (Receptor, Serotonin, 5-HT1A); 133025-23-7 (WAY 100135); 144425-84-3 (L 703606); 333DO1RDJY (Serotonin); 33507-63-0 (Substance P); 4091-50-3 (p-Methoxy-N-methylphenethylamine); 820484N8I3 (Histamine); BN34FX42G3 (allyl isothiocyanate); HPE317O9TL (Pyrilamine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161202
[St] Status:MEDLINE
[do] DOI:10.1007/s00011-016-1015-1



página 1 de 216 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde