Base de dados : MEDLINE
Pesquisa : D02.092.471.683.953.395 [Categoria DeCS]
Referências encontradas : 1119 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 112 ir para página                         

  1 / 1119 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27597056
[Au] Autor:Grigorieva DV; Gorudko IV; Sokolov AV; Kostevich VA; Vasilyev VB; Cherenkevich SN; Panasenko OM
[Ad] Endereço:Physics Faculty, Belarusian State University, Minsk, Belarus.
[Ti] Título:Myeloperoxidase Stimulates Neutrophil Degranulation.
[So] Source:Bull Exp Biol Med;161(4):495-500, 2016 Aug.
[Is] ISSN:1573-8221
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Myeloperoxidase, heme enzyme of azurophilic granules in neutrophils, is released into the extracellular space in the inflammation foci. In neutrophils, it stimulates a dose-dependent release of lactoferrin (a protein of specific granules), lysozyme (a protein of specific and azurophilic granules), and elastase (a protein of azurophilic granules). 4-Aminobenzoic acid hydrazide, a potent inhibitor of peroxidase activity of myeloperoxidase, produced no effect on neutrophil degranulation. Using signal transduction inhibitors (genistein, methoxyverapamil, wortmannin, and NiCl2), we demonstrated that myeloperoxidase-induced degranulation of neutrophils resulted from enzyme interaction with the plasma membrane and depends on activation of tyrosine kinases, phosphatidylinositol 3-kinases (PI3K), and calcium signaling. Myeloperoxidase modified by oxidative/halogenation stress (chlorinated and monomeric forms of the enzyme) lost the potency to activate neutrophil degranulation.
[Mh] Termos MeSH primário: Neutrófilos/metabolismo
Peroxidase/metabolismo
[Mh] Termos MeSH secundário: Ácido 4-Aminobenzoico/farmacologia
Androstadienos/farmacologia
Sinalização do Cálcio/efeitos dos fármacos
Degranulação Celular/efeitos dos fármacos
Células Cultivadas
Galopamil/farmacologia
Genisteína/farmacologia
Células HL-60
Seres Humanos
Neutrófilos/efeitos dos fármacos
Níquel/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Peroxidase/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Androstadienes); 39WPC8JHR8 (Gallopamil); 696BNE976J (nickel chloride); 7OV03QG267 (Nickel); DH2M523P0H (Genistein); EC 1.11.1.7 (Peroxidase); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); TL2TJE8QTX (4-Aminobenzoic Acid); XVA4O219QW (wortmannin)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170308
[Lr] Data última revisão:
170308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160907
[St] Status:MEDLINE
[do] DOI:10.1007/s10517-016-3446-7


  2 / 1119 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25876196
[Au] Autor:Sumino K; Sheshadri A; Castro M
[Ad] Endereço:1 Division of Pulmonary and Critical Care Medicine Washington University School of Medicine Saint Louis, Missouri and.
[Ti] Título:Calcium channel blocker reduces airway remodeling-or does it?
[So] Source:Am J Respir Crit Care Med;191(8):863-4, 2015 Apr 15.
[Is] ISSN:1535-4970
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Remodelação das Vias Aéreas/efeitos dos fármacos
Asma/tratamento farmacológico
Bloqueadores dos Canais de Cálcio/farmacologia
Galopamil/farmacologia
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:COMMENT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 39WPC8JHR8 (Gallopamil)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:150416
[Lr] Data última revisão:
150416
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150416
[St] Status:MEDLINE
[do] DOI:10.1164/rccm.201502-0322ED


  3 / 1119 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25791230
[Au] Autor:Aksoy-Aksel A; Manahan-Vaughan D
[Ad] Endereço:Department of Neurophysiology, Medical Faculty, Ruhr University Bochum, Germany; International Graduate School for Neuroscience, Ruhr University Bochum, Germany.
[Ti] Título:Synaptic strength at the temporoammonic input to the hippocampal CA1 region in vivo is regulated by NMDA receptors, metabotropic glutamate receptors and voltage-gated calcium channels.
[So] Source:Neuroscience;309:191-9, 2015 Nov 19.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The hippocampal CA1 region receives cortical information via two main inputs: directly via the perforant (temporoammonic) path (pp-CA1 synapse) and indirectly via the tri-synaptic pathway. Although synaptic plasticity has been reported at the pp-CA1 synapse of freely behaving animals, the mechanisms underlying this phenomenon have not been investigated. Here, we explored whether long-term potentiation (LTP) at the pp-CA1 synapse in freely behaving rats requires activation of N-methyl-d-aspartate receptors (NMDAR) and L-type voltage-gated calcium channels (VGCCs). As group II metabotropic glutamate (mGlu) receptors are densely localized on presynaptic terminals of the perforant path, and are important for certain forms of hippocampal synaptic plasticity, we also explored whether group II mGlu receptors affect LTP at the pp-CA1 synapse and/or regulate basal synaptic transmission at this synapse in vivo. In adult male rats, high-frequency stimulation (200Hz) given as 3, or 10 trains, resulted in robust LTP that lasted for at least 4h in pp-CA1 or pp-dentate gyrus (DG) synapses, respectively. Pre-treatment with the NMDAR antagonist D-(-)-2-amino-5-phosphopentanoic acid (D-AP5) partially inhibited LTP at pp-CA1, and completely prevented LTP at pp-DG synapses. Combined antagonism of NMDAR using D-AP5 and the VGCC inhibitor, (-)-methoxyverapamil hydrochloride elicited a further inhibition of the LTP response at pp-CA1 synapses. Whereas activation of group II mGlu receptors using (1R,2R)-3-((1S)-1-amino-2-hydroxy-2-oxoethyl) cyclopropane-1,2-dicarboxylic acid (DCG-IV) dose-dependently reduced basal synaptic transmission elicited by test-pulse stimulation, DCG-IV did not affect LTP in a dose that inhibited LTP at pp-DG synapses in vivo. These data indicate that LTP at the pp-CA1 synapse of freely behaving animals is dually dependent on NMDAR and VGCCs, whereby group II mGlu receptor activation affect basal synaptic tonus, but not LTP. The lower frequency-dependency of NMDA-VGCC LTP at pp-CA1 synapses compared to pp-DG synapses may comprise a mechanism to prioritize information processing at this synapse.
[Mh] Termos MeSH primário: Região CA1 Hipocampal/fisiologia
Canais de Cálcio Tipo L/metabolismo
Potenciação de Longa Duração/fisiologia
Receptores de Glutamato Metabotrópico/metabolismo
Receptores de N-Metil-D-Aspartato/metabolismo
Sinapses/fisiologia
[Mh] Termos MeSH secundário: Animais
Região CA1 Hipocampal/efeitos dos fármacos
Ciclopropanos/farmacologia
Giro Denteado/efeitos dos fármacos
Giro Denteado/fisiologia
Relação Dose-Resposta a Droga
Estimulação Elétrica
Eletrocorticografia
Eletrodos Implantados
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Potenciais Pós-Sinápticos Excitadores/fisiologia
Galopamil/farmacologia
Glicina/análogos & derivados
Glicina/farmacologia
Potenciação de Longa Duração/efeitos dos fármacos
Masculino
Neurotransmissores/farmacologia
Via Perfurante/efeitos dos fármacos
Via Perfurante/fisiologia
Ratos Wistar
Receptores de Glutamato Metabotrópico/antagonistas & inibidores
Receptores de N-Metil-D-Aspartato/antagonistas & inibidores
Sinapses/efeitos dos fármacos
Valina/análogos & derivados
Valina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Calcium Channels, L-Type); 0 (Cyclopropanes); 0 (Neurotransmitter Agents); 0 (Receptors, Metabotropic Glutamate); 0 (Receptors, N-Methyl-D-Aspartate); 147782-19-2 (2-(2,3-dicarboxycyclopropyl)glycine); 39WPC8JHR8 (Gallopamil); 76326-31-3 (2-amino-5-phosphopentanoic acid); HG18B9YRS7 (Valine); TE7660XO1C (Glycine)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:151102
[Lr] Data última revisão:
151102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150321
[St] Status:MEDLINE


  4 / 1119 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Registro de Ensaios Clínicos
Texto completo
[PMID]:25633090
[Au] Autor:Girodet PO; Dournes G; Thumerel M; Begueret H; Dos Santos P; Ozier A; Dupin I; Trian T; Montaudon M; Laurent F; Marthan R; Berger P
[Ad] Endereço:1 Université de Bordeaux, Centre de Recherche Cardio-thoracique de Bordeaux, U1045, Département de Pharmacologie, CIC1401, Bordeaux, France;
[Ti] Título:Calcium channel blocker reduces airway remodeling in severe asthma. A proof-of-concept study.
[So] Source:Am J Respir Crit Care Med;191(8):876-83, 2015 Apr 15.
[Is] ISSN:1535-4970
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Severe asthma is a major public health issue throughout the world. Increased bronchial smooth muscle (BSM) mass, a characteristic feature of airway remodeling in severe asthma, is associated with resistance to high-intensity treatment and poor prognosis. In vitro, the Ca(2+)-channel blocker gallopamil decreased the proliferation of BSM cells from patients with severe asthma. OBJECTIVES: We conducted a double-blind, randomized, placebo-controlled study to evaluate the effect of gallopamil on airway remodeling in patients with severe asthma. METHODS: Subjects received either gallopamil (n = 16) or placebo (n = 15) for 1 year and were monitored for an additional 3-month period. Airway remodeling was analyzed at baseline and after treatment phase using both fiberoptic bronchoscopy and computed tomography scan. The primary end point was the BSM area. Secondary end points included normalized BSM thickness and frequency of asthma exacerbations. MEASUREMENTS AND MAIN RESULTS: BSM area was reduced in the gallopamil group (baseline vs. end of treatment) but was unchanged in the placebo group. Between-group differences in BSM area were not significantly different in gallopamil versus placebo groups. By contrast, between-group differences in normalized BSM thickness were significantly different between the two groups. The mean number of exacerbations per month was not different during the treatment phase in gallopamil versus placebo group but was significantly lower in patients previously treated with gallopamil during the follow-up period. There were no differences between the groups with respect to overall side effects. CONCLUSIONS: Gallopamil treatment for 12 months reduces BSM remodeling and prevents the occurrence of asthma exacerbations. Clinical trial registered with www.clinicaltrials.gov (NCT 00896428).
[Mh] Termos MeSH primário: Remodelação das Vias Aéreas/efeitos dos fármacos
Asma/tratamento farmacológico
Bloqueadores dos Canais de Cálcio/farmacologia
Galopamil/farmacologia
[Mh] Termos MeSH secundário: Asma/diagnóstico por imagem
Broncografia/métodos
Broncoscopia/métodos
Método Duplo-Cego
Feminino
Tecnologia de Fibra Óptica
Seguimentos
Seres Humanos
Masculino
Meia-Idade
Tomografia Computadorizada por Raios X/métodos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 39WPC8JHR8 (Gallopamil)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150131
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE
[do] DOI:10.1164/rccm.201410-1874OC


  5 / 1119 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:19915583
[Au] Autor:Hayashi S; Hester RK
[Ad] Endereço:Department of Medical Pharmacology and Toxicology, and Microcirculation Research Institute, College of Medicine, Texas A&M University, College Station, TX 77843-1114, USA. s-hayashi@pha.ohu-u.ac.jp
[Ti] Título:Reduction in extracellular Ca2+ attenuates endothelium-dependent relaxation more than nitroprusside-induced relaxation.
[So] Source:Acta Pharmacol Sin;31(1):19-26, 2010 Jan.
[Is] ISSN:1745-7254
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:AIM: To quantitatively assess the effect of lowering external Ca(2+) ([Ca(2+)](o)) on both endothelium-dependent and -independent relaxations in rabbit aorta. METHODS: Isometric contractions and relaxations of isolated aortae were recorded. When assessing the effect of reduced [Ca(2+)](o) on relaxations, the normal [Ca(2+)](o) solution was substituted with one of the reduced [Ca(2+)](o) solutions for one aorta, while a paired aorta was replenished with normal [Ca(2+)](o) solution. RESULTS: The extent of acetylcholine (ACh)-induced relaxation, which is dependent on an intact endothelium, is time-dependent, and inversely related to [Ca(2+)](o) in a range of 0.02-2 mmol/L. ACh-induced relaxations were not significantly altered by the magnitude of the precontraction induced by PGF(2alpha). Nitroprusside-induced relaxations, which are independent of the endothelium, are also attenuated by reduced [Ca(2+)](o). Relaxant responses to ACh were significantly more susceptible to reduced [Ca(2+)](o) than nitroprusside-induced relaxations. A maximally effective relaxing concentration of D600, an L-type Ca channel blocker methoxyverapamil, (10(-5) mol/L) attenuated ACh-induced relaxations, whereas nitroprusside-induced relaxations were unaffected by D600. CONCLUSION: Thus, endothelium-dependent relaxation is more dependent on [Ca(2+)](o) than endothelium-independent relaxation, and it seems likely that [Ca(2+)](o) plays an important role not only in contractile processes, but also in relaxant processes as well.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Nitroprussiato/farmacologia
Vasodilatação/efeitos dos fármacos
Vasodilatadores/farmacologia
[Mh] Termos MeSH secundário: Acetilcolina/farmacologia
Animais
Aorta/efeitos dos fármacos
Aorta/metabolismo
Bloqueadores dos Canais de Cálcio/farmacologia
Canais de Cálcio Tipo L/efeitos dos fármacos
Canais de Cálcio Tipo L/metabolismo
Dinoprosta/farmacologia
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/metabolismo
Feminino
Galopamil/farmacologia
Técnicas In Vitro
Contração Isométrica/efeitos dos fármacos
Masculino
Coelhos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Calcium Channels, L-Type); 0 (Vasodilator Agents); 169D1260KM (Nitroprusside); 39WPC8JHR8 (Gallopamil); B7IN85G1HY (Dinoprost); N9YNS0M02X (Acetylcholine); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1003
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:091117
[St] Status:MEDLINE
[do] DOI:10.1038/aps.2009.164


  6 / 1119 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:19700404
[Au] Autor:Cheng RC; Tikhonov DB; Zhorov BS
[Ad] Endereço:Department of Biochemistry and Biomedical Sciences, McMaster University, Hamilton, Ontario L8N 3Z5, Canada.
[Ti] Título:Structural model for phenylalkylamine binding to L-type calcium channels.
[So] Source:J Biol Chem;284(41):28332-42, 2009 Oct 09.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Phenylalkylamines (PAAs), a major class of L-type calcium channel (LTCC) blockers, have two aromatic rings connected by a flexible chain with a nitrile substituent. Structural aspects of ligand-channel interactions remain unclear. We have built a KvAP-based model of LTCC and used Monte Carlo energy minimizations to dock devapamil, verapamil, gallopamil, and other PAAs. The PAA-LTCC models have the following common features: (i) the meta-methoxy group in ring A, which is proximal to the nitrile group, accepts an H-bond from a PAA-sensing Tyr_IIIS6; (ii) the meta-methoxy group in ring B accepts an H-bond from a PAA-sensing Tyr_IVS6; (iii) the ammonium group is stabilized at the focus of P-helices; and (iv) the nitrile group binds to a Ca(2+) ion coordinated by the selectivity filter glutamates in repeats III and IV. The latter feature can explain Ca(2+) potentiation of PAA action and the presence of an electronegative atom at a similar position of potent PAA analogs. Tyr substitution of a Thr in IIIS5 is known to enhance action of devapamil and verapamil. Our models predict that the para-methoxy group in ring A of devapamil and verapamil accepts an H-bond from this engineered Tyr. The model explains structure-activity relationships of PAAs, effects of LTCC mutations on PAA potency, data on PAA access to LTCC, and Ca(2+) potentiation of PAA action. Common and class-specific aspects of action of PAAs, dihydropyridines, and benzothiazepines are discussed in view of the repeat interface concept.
[Mh] Termos MeSH primário: Bloqueadores dos Canais de Cálcio
Canais de Cálcio Tipo L/química
Canais de Cálcio Tipo L/metabolismo
Modelos Moleculares
Estrutura Terciária de Proteína
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Sítios de Ligação
Bloqueadores dos Canais de Cálcio/química
Bloqueadores dos Canais de Cálcio/metabolismo
Canais de Cálcio Tipo L/genética
Simulação por Computador
Di-Hidropiridinas/química
Galopamil/química
Galopamil/metabolismo
Dados de Sequência Molecular
Estrutura Molecular
Método de Monte Carlo
Alinhamento de Sequência
Relação Estrutura-Atividade
Verapamil/análogos & derivados
Verapamil/química
Verapamil/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Calcium Channels, L-Type); 0 (Dihydropyridines); 39WPC8JHR8 (Gallopamil); CJ0O37KU29 (Verapamil); M6142PTV7J (devapamil)
[Em] Mês de entrada:0911
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090825
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M109.027326


  7 / 1119 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:19176761
[Au] Autor:Matsuoka H; Harada K; Ikeda T; Uetsuki K; Sata T; Warashina A; Inoue M
[Ad] Endereço:Dept. of Cell and Systems Physiology, School of Medicine, Univ. of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.
[Ti] Título:Ca2+ pathway involved in the refilling of store sites in rat adrenal medullary cells.
[So] Source:Am J Physiol Cell Physiol;296(4):C889-99, 2009 Apr.
[Is] ISSN:0363-6143
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It has been suggested that store-operated Ca(2+) entry (SOC) facilitates catecholamine secretion and synthesis in bovine adrenal medullary (AM) cells. However, there has been no experimental result clearly showing that cation channel activity is enhanced by store Ca(2+) depletion. Thus the present experiments were undertaken to address the issue of whether rat AM cells have SOC channels. Inhibition of the sarco(endo)plasmic reticulum Ca(2+) (SERCA) pump resulted in a sustained increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) in rat AM cells. This increase was completely suppressed by 2 mM Ni(2+) but not by 100 muM D600. A bath application of Ni(2+), but not D600, produced an outward current at -60 mV in rat AM cells, whereas exposure to a SERCA pump inhibitor did not affect either the whole cell current level or the Ni(2+)-induced outward current. The refilling of intracellular store sites was suppressed by the addition of Ni(2+) to the perfusate. RT-PCR revealed that transcripts for transient receptor potential channels 1 (TRPC1) and 5 (TRPC5) were present in rat adrenal medullas. Immunocytochemistry showed that TRPC1 channels, which have been implicated in SOC in certain types of cells, were mainly localized in the endoplasmic reticulum (ER) and not in the plasma membrane, and that STIM1, a Ca(2+) sensor in the ER, was not expressed in rat AM cells. On the basis of these results, we conclude that rat AM cells lack the SOC mechanism.
[Mh] Termos MeSH primário: Medula Suprarrenal/metabolismo
Canais de Cálcio/metabolismo
Sinalização do Cálcio
Cálcio/metabolismo
[Mh] Termos MeSH secundário: Medula Suprarrenal/efeitos dos fármacos
Medula Suprarrenal/secreção
Animais
Bloqueadores dos Canais de Cálcio/farmacologia
Canais de Cálcio/efeitos dos fármacos
Canais de Cálcio/genética
Sinalização do Cálcio/efeitos dos fármacos
Catecolaminas/secreção
Membrana Celular/metabolismo
Estimulação Elétrica
Retículo Endoplasmático/metabolismo
Inibidores Enzimáticos/farmacologia
Galopamil/farmacologia
Indóis/farmacologia
Masculino
Glicoproteínas de Membrana/metabolismo
Potenciais da Membrana
Níquel/metabolismo
RNA Mensageiro/metabolismo
Ratos
Ratos Wistar
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/antagonistas & inibidores
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/metabolismo
Molécula 1 de Interação Estromal
Canais de Cátion TRPC/metabolismo
Tapsigargina/farmacologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Calcium Channels); 0 (Catecholamines); 0 (Enzyme Inhibitors); 0 (Indoles); 0 (Membrane Glycoproteins); 0 (RNA, Messenger); 0 (Stim1 protein, rat); 0 (Stromal Interaction Molecule 1); 0 (TRPC Cation Channels); 0 (Trpc5 protein, rat); 0 (transient receptor potential cation channel, subfamily C, member 1); 39WPC8JHR8 (Gallopamil); 67526-95-8 (Thapsigargin); 7OV03QG267 (Nickel); EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases); SY7Q814VUP (Calcium); X9TLY4580Z (cyclopiazonic acid)
[Em] Mês de entrada:0906
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090130
[St] Status:MEDLINE
[do] DOI:10.1152/ajpcell.00439.2008


  8 / 1119 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:17651721
[Au] Autor:Tarabova B; Lacinova L; Engel J
[Ad] Endereço:Slovak Academy of Sciences, Institute of Molecular Physiology and Genetics, Vlárska 5, 833 34 Bratislava, Slovak Republic. bohumila.tarabova@savba.sk
[Ti] Título:Effects of phenylalkylamines and benzothiazepines on Ca(v)1.3-mediated Ca2+ currents in neonatal mouse inner hair cells.
[So] Source:Eur J Pharmacol;573(1-3):39-48, 2007 Nov 14.
[Is] ISSN:0014-2999
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Calcium currents (I(Ca)) in inner hair cells (IHCs) are carried by the Ca(v)1.3 subtype of L-type calcium channels. They play an important role in synaptic transmission of sound-evoked mechanical stimuli. L-type calcium channels are targets of the organic blocker classes dihydropyridines, phenylalkylamines and benzothiazepines. Previously a low sensitivity of the Ca(v)1.3 subtype towards dihydropyridines has been demonstrated. Therefore, this study evaluates the effect of two phenylalkylamines (verapamil and gallopamil) and the benzothiazepine diltiazem on I(Ca) through Ca(v)1.3 channels in mouse IHCs. Whole-cell I(Ca) was measured using the patch-clamp technique in mouse IHCs aged postnatal day 3-7 with 5 mM calcium as a charge carrier. The phenylalkylamines verapamil and gallopamil and the benzothiazepine diltiazem inhibited I(Ca) in IHCs in a concentration-dependent manner. This block was largely reversible. Dose-response curves revealed IC(50) values of 199+/-19 microM for verapamil, 466+/-151 microM for gallopamil and 326+/-67 microM for diltiazem. The inhibition of peak I(Ca) by phenylalkylamines and benzothiazepines was voltage-independent. Verapamil (300 microM) enhanced current inactivation from -20 to +20 mV while diltiazem (300 microM) did so only at very depolarised potentials (+20 mV). In conclusion, the concentrations of phenylalkylamines and benzothiazepine necessary to inhibit 50% of I(Ca) in IHCs were one order larger compared to concentrations which inhibited I(Ca) through Ca(v)1.2 channels in native cells or expression systems. However, inhibitory concentrations were in the same range as those required for block of I(Ca) in turtle hair cells.
[Mh] Termos MeSH primário: Benzazepinas/farmacologia
Canais de Cálcio Tipo L/fisiologia
Células Ciliadas Auditivas Internas/efeitos dos fármacos
Fenetilaminas/farmacologia
[Mh] Termos MeSH secundário: Algoritmos
Animais
Animais Recém-Nascidos
Bloqueadores dos Canais de Cálcio/farmacologia
Sinalização do Cálcio/efeitos dos fármacos
Diltiazem/farmacologia
Relação Dose-Resposta a Droga
Galopamil/farmacologia
Células Ciliadas Auditivas Internas/citologia
Células Ciliadas Auditivas Internas/fisiologia
Potenciais da Membrana/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos
Verapamil/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Benzazepines); 0 (Calcium Channel Blockers); 0 (Calcium Channels, L-Type); 0 (Phenethylamines); 39WPC8JHR8 (Gallopamil); CJ0O37KU29 (Verapamil); EE92BBP03H (Diltiazem)
[Em] Mês de entrada:0803
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070727
[St] Status:MEDLINE


  9 / 1119 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:17626204
[Au] Autor:Makani S; Chesler M
[Ad] Endereço:Department of Neurosurgery, New York University School of Medicine, New York, New York 10016, USA.
[Ti] Título:Endogenous alkaline transients boost postsynaptic NMDA receptor responses in hippocampal CA1 pyramidal neurons.
[So] Source:J Neurosci;27(28):7438-46, 2007 Jul 11.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In hippocampus, activation of the Schaffer collaterals generates an extracellular alkaline transient both in vitro and in vivo. This pH change may provide relief of the H+ block of NMDA receptors (NMDARs) and thereby increase excitability. To test this hypothesis, we augmented extracellular buffering in mouse hippocampal slices by adding 2 microM bovine type II carbonic anhydrase to the superfusate. With addition of enzyme, the alkaline transient elicited by a 10 pulse, 100 Hz stimulus train was reduced by 33%. At a holding potential (V(H)) of -30 mV, the enzyme decreased the half-time of decay and charge transfer of EPSCs by 32 and 39%, respectively, but had no effect at a V(H) of -80 mV. In current clamp, a 10 pulse, 100 Hz stimulus train gave rise to an NMDAR-dependent afterdepolarization (ADP). Exogenous enzyme curtailed the ADP half-width and voltage integral by 20 and 25%, respectively. Similar reduction of the ADP was noted with a brief 12 Hz stimulus train. The effect persisted in the presence of GABAergic antagonists or the L-type Ca2+ channel blocker methoxyverapamil hydrochloride but was absent in the presence of the carbonic anhydrase inhibitor benzolamide or when the exogenous enzyme was heat inactivated. The effects of the enzyme in voltage and current clamp were noted in 0 Mg2+ media but were abolished when (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]-cyclohepten-5,10-imine maleate was included in the patch pipette. These results provide strong evidence that endogenous alkaline transients are sufficiently large in the vicinity of the synapse to augment NMDAR responses.
[Mh] Termos MeSH primário: Álcalis/metabolismo
Hipocampo/metabolismo
Células Piramidais/metabolismo
Receptores de N-Metil-D-Aspartato/metabolismo
Sinapses/metabolismo
[Mh] Termos MeSH secundário: Potenciais de Ação
Álcalis/antagonistas & inibidores
Animais
Benzolamida/farmacologia
Bloqueadores dos Canais de Cálcio/farmacologia
Canais de Cálcio Tipo L/efeitos dos fármacos
Inibidores da Anidrase Carbônica/farmacologia
Anidrases Carbônicas/farmacologia
Estimulação Elétrica
Eletrofisiologia
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Feminino
Antagonistas GABAérgicos/farmacologia
Galopamil/farmacologia
Hipocampo/fisiologia
Técnicas In Vitro
Isoenzimas/farmacologia
Masculino
Camundongos
Técnicas de Patch-Clamp
Células Piramidais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Alkalies); 0 (Calcium Channel Blockers); 0 (Calcium Channels, L-Type); 0 (Carbonic Anhydrase Inhibitors); 0 (GABA Antagonists); 0 (Isoenzymes); 0 (Receptors, N-Methyl-D-Aspartate); 39WPC8JHR8 (Gallopamil); EC 4.2.1.1 (Carbonic Anhydrases); FC5AAH89R5 (Benzolamide)
[Em] Mês de entrada:0708
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070713
[St] Status:MEDLINE


  10 / 1119 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
[PMID]:17357983
[Au] Autor:Stefanova ID; Argirova MD; Krustev AD
[Ad] Endereço:Department of Biophysics, Medical University, Plovdiv, Bulgaria.
[Ti] Título:Influence of model melanoidins on calcium-dependent transport mechanisms in smooth muscle tissue.
[So] Source:Mol Nutr Food Res;51(4):468-72, 2007 Apr.
[Is] ISSN:1613-4125
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Melanoidins obtained from L-arginine and D-glucose (MW > 3500 Da) were tested for their ability to influence the contractility of gastric smooth muscles. A study within the range 0.1-10 mg/mL revealed that at low concentrations, the melanoidins provoked concentration-dependent contraction, whereas a muscle relaxation was registered at high concentrations. The contraction was preceded by changes in the calcium membrane current as measured by single sucrose-gap method and significantly attenuated by the calcium channel blockers D-600 and nifedipine. Measurements with Ca(2+)-selective electrode showed that the melanoidins decreased the concentration of ionized Ca(2+ )in tissue bath in concentration-dependent manner. Experiments carried out in solutions with lower than normal Ca(2+) concentration and using melanoidins preliminary saturated with Ca(2+ )confirmed that the calcium chelation by melanoidins was a key contributing cause for the development of relaxant response. The results obtained showed that the melanoidins could influence the contractility of smooth muscles through at least two pathways: at low concentrations they caused depolarization and activation of L-type calcium channels, stimulated the Ca(2+ )influx, and provoked contraction, whereas at high concentrations calcium binding by melanoidins led to significant depletion of extracellular calcium ions and contributed to the relaxation process observed.
[Mh] Termos MeSH primário: Cálcio/fisiologia
Músculo Liso/efeitos dos fármacos
Músculo Liso/metabolismo
Polímeros/farmacologia
[Mh] Termos MeSH secundário: Animais
Arginina/farmacologia
Transporte Biológico/efeitos dos fármacos
Cálcio/análise
Bloqueadores dos Canais de Cálcio/farmacologia
Condutividade Elétrica
Galopamil/farmacologia
Glucose/farmacologia
Soluções Isotônicas
Masculino
Contração Muscular/efeitos dos fármacos
Nifedipino/farmacologia
Cloreto de Potássio/farmacologia
Ratos
Ratos Wistar
Estômago
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Isotonic Solutions); 0 (Krebs-Ringer solution); 0 (Polymers); 0 (melanoidin polymers); 39WPC8JHR8 (Gallopamil); 660YQ98I10 (Potassium Chloride); 94ZLA3W45F (Arginine); I9ZF7L6G2L (Nifedipine); IY9XDZ35W2 (Glucose); SY7Q814VUP (Calcium)
[Em] Mês de entrada:0707
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:070316
[St] Status:MEDLINE



página 1 de 112 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