Base de dados : MEDLINE
Pesquisa : D12.776.543.750.670.300 [Categoria DeCS]
Referências encontradas : 205 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 21 ir para página                         

  1 / 205 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26711850
[Au] Autor:Osier ND; Dixon CE
[Ad] Endereço:Safar Center for Resuscitation Research, University of Pittsburgh, Pittsburgh, PA 15213, USA; School of Nursing, University of Pittsburgh, Pittsburgh, PA 15213, USA.
[Ti] Título:Catecholaminergic based therapies for functional recovery after TBI.
[So] Source:Brain Res;1640(Pt A):15-35, 2016 Jun 01.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Among the many pathophysiologic consequences of traumatic brain injury are changes in catecholamines, including dopamine, epinephrine, and norepinephrine. In the context of TBI, dopamine is the one most extensively studied, though some research exploring epinephrine and norepinephrine have also been published. The purpose of this review is to summarize the evidence surrounding use of drugs that target the catecholaminergic system on pathophysiological and functional outcomes of TBI using published evidence from pre-clinical and clinical brain injury studies. Evidence of the effects of specific drugs that target catecholamines as agonists or antagonists will be discussed. Taken together, available evidence suggests that therapies targeting the catecholaminergic system may attenuate functional deficits after TBI. Notably, it is fairly common for TBI patients to be treated with catecholamine agonists for either physiological symptoms of TBI (e.g. altered cerebral perfusion pressures) or a co-occuring condition (e.g. shock), or cognitive symptoms (e.g. attentional and arousal deficits). Previous clinical trials are limited by methodological limitations, failure to replicate findings, challenges translating therapies to clinical practice, the complexity or lack of specificity of catecholamine receptors, as well as potentially counfounding effects of personal and genetic factors. Overall, there is a need for additional research evidence, along with a need for systematic dissemination of important study details and results as outlined in the common data elements published by the National Institute of Neurological Diseases and Stroke. Ultimately, a better understanding of catecholamines in the context of TBI may lead to therapeutic advancements. This article is part of a Special Issue entitled SI:Brain injury and recovery.
[Mh] Termos MeSH primário: Lesões Encefálicas Traumáticas/tratamento farmacológico
Lesões Encefálicas Traumáticas/metabolismo
Catecolaminas/metabolismo
Neurotransmissores/uso terapêutico
Recuperação de Função Fisiológica/efeitos dos fármacos
Recuperação de Função Fisiológica/fisiologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Fármacos Neuroprotetores/farmacologia
Fármacos Neuroprotetores/uso terapêutico
Neurotransmissores/farmacologia
Receptores de Catecolaminas/agonistas
Receptores de Catecolaminas/antagonistas & inibidores
Receptores de Catecolaminas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Catecholamines); 0 (Neuroprotective Agents); 0 (Neurotransmitter Agents); 0 (Receptors, Catecholamine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151230
[St] Status:MEDLINE


  2 / 205 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26371128
[Au] Autor:Brickman TJ; Suhadolc RJ; Armstrong SK
[Ad] Endereço:Department of Microbiology and Immunology, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
[Ti] Título:Interspecies variations in Bordetella catecholamine receptor gene regulation and function.
[So] Source:Infect Immun;83(12):4639-52, 2015 Dec.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bordetella bronchiseptica can use catecholamines to obtain iron from transferrin and lactoferrin via uptake pathways involving the BfrA, BfrD, and BfrE outer membrane receptor proteins, and although Bordetella pertussis has the bfrD and bfrE genes, the role of these genes in iron uptake has not been demonstrated. In this study, the bfrD and bfrE genes of B. pertussis were shown to be functional in B. bronchiseptica, but neither B. bronchiseptica bfrD nor bfrE imparted catecholamine utilization to B. pertussis. Gene fusion analyses found that expression of B. bronchiseptica bfrA was increased during iron starvation, as is common for iron receptor genes, but that expression of the bfrD and bfrE genes of both species was decreased during iron limitation. As shown previously for B. pertussis, bfrD expression in B. bronchiseptica was also dependent on the BvgAS virulence regulatory system; however, in contrast to the case in B. pertussis, the known modulators nicotinic acid and sulfate, which silence Bvg-activated genes, did not silence expression of bfrD in B. bronchiseptica. Further studies using a B. bronchiseptica bvgAS mutant expressing the B. pertussis bvgAS genes revealed that the interspecies differences in bfrD modulation are partly due to BvgAS differences. Mouse respiratory infection experiments determined that catecholamine utilization contributes to the in vivo fitness of B. bronchiseptica and B. pertussis. Additional evidence of the in vivo importance of the B. pertussis receptors was obtained from serologic studies demonstrating pertussis patient serum reactivity with the B. pertussis BfrD and BfrE proteins.
[Mh] Termos MeSH primário: Proteínas da Membrana Bacteriana Externa/imunologia
Infecções por Bordetella/imunologia
Bordetella bronchiseptica/patogenicidade
Bordetella pertussis/patogenicidade
Regulação Bacteriana da Expressão Gênica
Receptores de Catecolaminas/imunologia
Receptores de Superfície Celular/imunologia
[Mh] Termos MeSH secundário: Animais
Proteínas da Membrana Bacteriana Externa/genética
Proteínas de Bactérias/genética
Proteínas de Bactérias/imunologia
Infecções por Bordetella/microbiologia
Infecções por Bordetella/patologia
Bordetella bronchiseptica/genética
Bordetella bronchiseptica/imunologia
Bordetella bronchiseptica/metabolismo
Bordetella pertussis/genética
Bordetella pertussis/imunologia
Bordetella pertussis/metabolismo
Catecolaminas/imunologia
Catecolaminas/metabolismo
Seres Humanos
Ferro/imunologia
Ferro/metabolismo
Camundongos
Camundongos Endogâmicos BALB C
Isoformas de Proteínas/genética
Isoformas de Proteínas/imunologia
Receptores de Catecolaminas/genética
Receptores de Superfície Celular/genética
Sideróforos/imunologia
Sideróforos/metabolismo
Especificidade da Espécie
Fatores de Transcrição/genética
Fatores de Transcrição/imunologia
Virulência
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Bacterial Outer Membrane Proteins); 0 (Bacterial Proteins); 0 (BfrA protein, Bordetella bronchiseptica); 0 (BvgA protein, Bacteria); 0 (Catecholamines); 0 (Protein Isoforms); 0 (Receptors, Catecholamine); 0 (Receptors, Cell Surface); 0 (Siderophores); 0 (Transcription Factors); 0 (bvgS protein, Bordetella pertussis); E1UOL152H7 (Iron)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150916
[St] Status:MEDLINE
[do] DOI:10.1128/IAI.00787-15


  3 / 205 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26332355
[Au] Autor:Conceição EP; Moura EG; Carvalho JC; Oliveira E; Lisboa PC
[Ad] Endereço:Laboratory of Endocrine Physiology, Department of Physiological Sciences, Roberto Alcantara Gomes Biology Institute, State University of Rio de Janeiro, RJ, Brazil.
[Ti] Título:Early redox imbalance is associated with liver dysfunction at weaning in overfed rats.
[So] Source:J Physiol;593(21):4799-811, 2015 Nov 01.
[Is] ISSN:1469-7793
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Neonatal overfeeding induced by litter size reduction leads to further obesity and other metabolic disorders, such as liver oxidative stress and microsteatosis at adulthood. We hypothesized that overfeeding causes an early redox imbalance at weaning, which could programme the animals to future liver dysfunction. Thus, we studied lipogenesis, adipogenesis, catecholamine status and oxidative balance in weaned overfed pups. To induce early overfeeding, litters were adjusted to three pups at the 3rd day of lactation (SL group). The control group contained 10 pups per litter until weaning (NL group). Peripheral autonomic nerve function was determined in vivo at 21 days old. Thereafter, pups were killed for further analysis. Differences were considered significant when P < 0.05. The SL pups presented with a higher visceral adipocyte area, higher content of lipogenic enzymes (ACC, FAS) and with a lower content of adipogenic factors (CEBP, PPARγ) in visceral adipose tissue (VAT). Although autonomic nerve activity and adrenal catecholamine production were not significantly altered, catecholamine receptor (ß3ADR) content was lower in VAT. The SL pups also presented with higher triglyceride, PPARγ, PPARα and PGC1α contents in liver. In plasma and liver, the SL pups showed an oxidative imbalance, with higher lipid peroxidation and protein oxidation. The SL group presented with a higher serum alanine aminotransferase (ALT). The early increase in lipogenesis in adipose tissue and liver in weaned overfed rats suggests that the higher oxidative stress and lower catecholamine content in VAT are associated with the early development of liver dysfunction and adipocyte hypertrophy.
[Mh] Termos MeSH primário: Hiperfagia/metabolismo
Fígado/metabolismo
Obesidade/metabolismo
Estresse Oxidativo
[Mh] Termos MeSH secundário: Adipócitos/metabolismo
Adipócitos/patologia
Animais
Catecolaminas/metabolismo
Feminino
Lipogênese
Fígado/crescimento & desenvolvimento
Masculino
PPAR gama/metabolismo
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo
Ratos
Ratos Wistar
Receptores de Catecolaminas/metabolismo
Fatores de Transcrição/metabolismo
Triglicerídeos/metabolismo
Desmame
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Catecholamines); 0 (PPAR gamma); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (Ppargc1a protein, rat); 0 (Receptors, Catecholamine); 0 (Transcription Factors); 0 (Triglycerides)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150903
[St] Status:MEDLINE
[do] DOI:10.1113/JP271189


  4 / 205 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25790933
[Au] Autor:Armand-Ugón M; Aso E; Moreno J; Riera-Codina M; Sánchez A; Vegas E; Ferrer I
[Ad] Endereço:Institut de Neuropatologia, IDIBELL-Hospital Universitari de Bellvitge, Universitat de Barcelona, L'Hospitalet de Llobregat, Spain. marmand@idibell.cat
[Ti] Título:Memory Improvement in the AßPP/PS1 Mouse Model of Familial Alzheimer's Disease Induced by Carbamylated-Erythropoietin is Accompanied by Modulation of Synaptic Genes.
[So] Source:J Alzheimers Dis;45(2):407-21, 2015.
[Is] ISSN:1875-8908
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Neuroprotection of erythropoietin (EPO) following long-term administration is hampered by the associated undesirable effects on hematopoiesis and body weight. For this reason, we tested carbamylated-EPO (CEPO), which has no effect on erythropoiesis, and compared it with EPO in the AßPP/PS1 mouse model of familial Alzheimer's disease. Groups of 5-month old wild type (WT) and transgenic mice received chronic treatment consisting of CEPO (2,500 or 5,000 UI/kg) or EPO (2,500 U I/kg) 3 days/week for 4 weeks. Memory at the end of treatment was assessed with the object recognition test. Microarray analysis and quantitative-PCR were used for gene expression studies. No alterations in erythropoiesis were observed in CEPO-treated WT and AßPP/PS1 transgenic mice. EPO and CEPO improved memory in AßPP/PS1 animals. However, only EPO decreased amyloid-ß (Aß)plaque burden and soluble Aß(40). Microarray analysis of gene expression revealed a limited number of common genes modulated by EPO and CEPO. CEPO but not EPO significantly increased gene expression of dopamine receptors 1 and 2, and adenosine receptor 2a, and significantly down-regulated adrenergic receptor 1D and gastrin releasing peptide. CEPO treatment resulted in higher protein levels of dopamine receptors 1 and 2 in WT and AßPP/PS1 animals, whereas the adenosine receptor 2a was reduced in WT animals. The present results suggest that the improved behavior observed in AßPP/PS1 transgenic mice after CEPO treatment may be mediated, at least in part, by the observed modulation of the expression of molecules involved in neurotransmission.
[Mh] Termos MeSH primário: Doença de Alzheimer/complicações
Eritropoetina/análogos & derivados
Regulação da Expressão Gênica/efeitos dos fármacos
Transtornos da Memória/tratamento farmacológico
Transtornos da Memória/etiologia
Sinapses/metabolismo
[Mh] Termos MeSH secundário: Doença de Alzheimer/genética
Peptídeos beta-Amiloides/metabolismo
Precursor de Proteína beta-Amiloide/genética
Animais
Peso Corporal/efeitos dos fármacos
Peso Corporal/genética
Modelos Animais de Doenças
Eritropoetina/uso terapêutico
Peptídeo Liberador de Gastrina/metabolismo
Regulação da Expressão Gênica/genética
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Mutação/genética
Fragmentos de Peptídeos/metabolismo
Presenilina-1/genética
Receptores de Catecolaminas/metabolismo
Sinapses/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Amyloid beta-Protein Precursor); 0 (PSEN1 protein, human); 0 (Peptide Fragments); 0 (Presenilin-1); 0 (Receptors, Catecholamine); 0 (amyloid beta-protein (1-40)); 0 (amyloid beta-protein (1-42)); 0 (carbamylated erythropoietin); 11096-26-7 (Erythropoietin); 80043-53-4 (Gastrin-Releasing Peptide)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:150320
[Lr] Data última revisão:
150320
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150321
[St] Status:MEDLINE
[do] DOI:10.3233/JAD-150002


  5 / 205 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25572531
[Au] Autor:Di Miceli M; Gronier B
[Ad] Endereço:Leicester School of Pharmacy, De Montfort University, The Gateway, Leicester, LE1 9BH, UK.
[Ti] Título:Psychostimulants and atomoxetine alter the electrophysiological activity of prefrontal cortex neurons, interaction with catecholamine and glutamate NMDA receptors.
[So] Source:Psychopharmacology (Berl);232(12):2191-205, 2015 Jun.
[Is] ISSN:1432-2072
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Attention-deficit hyperactivity disorder (ADHD) is the most frequently diagnosed neuropsychiatric disorder in childhood. Currently available ADHD drugs include the psychostimulants methylphenidate (MPH) and D-amphetamine (D-AMP), acting on norepinephrine and dopamine transporters/release, and atomoxetine (ATX), a selective norepinephrine uptake inhibitor. Recent evidence suggests an involvement of glutamate neurotransmission in the pathology and treatment of ADHD, via mechanisms to be clarified. OBJECTIVE: We have investigated how ADHD drugs could modulate, through interaction with catecholamine receptors, basal and glutamate-induced excitability of pyramidal neurons in the prefrontal cortex (PFC), a region which plays a major role in control of attention and impulsivity. METHODS: We have used the technique of extracellular single-unit recording in anaesthetised rats coupled with microiontophoresis. RESULTS: Both MPH (1-3 mg/kg) and D-AMP (1-9 mg/kg) increased the firing activity of PFC neurons in a dopamine D1 receptor-dependent manner. ATX administration (1-6 mg/kg) also increased the firing of neurons, but this effect is not significantly reversed by D1 (SCH 23390) or alpha1 (prazosin) receptor antagonists but potentiated by alpha2 antagonist (yohimbine). All drugs induced a clear potentiation of the excitatory response of PFC neurons to the microiontophoretic application of the glutamate agonist N-methyl-D-aspartate (NMDA), but not to the glutamate agonist α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). The potentiating effect of D-AMP on NMDA-induced activation of PFC neurons was partially reversed or prevented by dopamine D1 receptor blockade. CONCLUSION: Our data shows that increase in excitability of PFC neurons in basal conditions and via NMDA receptor activation may be involved in the therapeutic response to ADHD drugs.
[Mh] Termos MeSH primário: Cloridrato de Atomoxetina/farmacologia
Estimulantes do Sistema Nervoso Central/farmacologia
Neurônios/efeitos dos fármacos
Córtex Pré-Frontal/efeitos dos fármacos
Receptores de Catecolaminas/efeitos dos fármacos
Receptores de N-Metil-D-Aspartato/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Relação Dose-Resposta a Droga
Fenômenos Eletrofisiológicos/efeitos dos fármacos
Masculino
Metilfenidato/farmacologia
Córtex Pré-Frontal/citologia
Células Piramidais/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Receptores de AMPA/efeitos dos fármacos
Receptores de Dopamina D1/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Central Nervous System Stimulants); 0 (Receptors, AMPA); 0 (Receptors, Catecholamine); 0 (Receptors, Dopamine D1); 0 (Receptors, N-Methyl-D-Aspartate); 207ZZ9QZ49 (Methylphenidate); 57WVB6I2W0 (Atomoxetine Hydrochloride)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150110
[St] Status:MEDLINE
[do] DOI:10.1007/s00213-014-3849-y


  6 / 205 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:24925409
[Au] Autor:Starke K
[Ad] Endereço:Department of Experimental and Clinical Pharmacology and Toxicology, Albert-Ludwigs-Universität, Freiburg im Breisgau, Germany.
[Ti] Título:History of catecholamine research.
[So] Source:Chem Immunol Allergy;100:288-301, 2014.
[Is] ISSN:1662-2898
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The prominence of catecholamines and their congeners in allergic diseases rests chiefly on their use in asthma and acute hypersensitivity reactions, such as anaphylaxis. They act in these indications by activating both α- and ß-adrenoceptors. Adrenaline, the prototype, was discovered in the adrenals in 1893/1894. In 1939, dopa decarboxylase was the first enzyme in the biosynthesis of catecholamines to be described. Later other catecholamines like noradrenaline and dopamine were characterized. The identification of the active chemicals went along with studies regarding catecholamine receptors. It took until 1948 before the existence of at least two different receptors for the different effects was accepted. Meanwhile, genes from all mammalian catecholamine receptors have been cloned.
[Mh] Termos MeSH primário: Anafilaxia/tratamento farmacológico
Asma/tratamento farmacológico
Catecolaminas/uso terapêutico
[Mh] Termos MeSH secundário: Medula Suprarrenal/metabolismo
Catecolaminas/história
Catecolaminas/metabolismo
Dopa Descarboxilase/metabolismo
Epinefrina/história
Epinefrina/metabolismo
História do Século XIX
História do Século XX
Seres Humanos
Neurotransmissores/química
Neurotransmissores/uso terapêutico
Receptores de Catecolaminas/metabolismo
[Pt] Tipo de publicação:HISTORICAL ARTICLE; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catecholamines); 0 (Neurotransmitter Agents); 0 (Receptors, Catecholamine); EC 4.1.1.- (Dopa Decarboxylase); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:140613
[Lr] Data última revisão:
140613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140614
[St] Status:MEDLINE
[do] DOI:10.1159/000359962


  7 / 205 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:24916280
[Au] Autor:Fujita W; Gomes I; Devi LA
[Ad] Endereço:Department of Pharmacology and Systems Therapeutics, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
[Ti] Título:Revolution in GPCR signalling: opioid receptor heteromers as novel therapeutic targets: IUPHAR review 10.
[So] Source:Br J Pharmacol;171(18):4155-76, 2014 Sep.
[Is] ISSN:1476-5381
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:GPCRs can interact with each other to form homomers or heteromers. Homomers involve interactions with the same receptor type while heteromers involve interactions between two different GPCRs. These receptor-receptor interactions modulate not only the binding but also the signalling and trafficking properties of individual receptors. Opioid receptor heteromerization has been extensively investigated with the objective of identifying novel therapeutic targets that are as potent as morphine but without the side effects associated with chronic morphine use. In this context, studies have described heteromerization between the different types of opioid receptors and between opioid receptors and a wide range of GPCRs including adrenoceptors, cannabinoid, 5-HT, metabotropic glutamate and sensory neuron-specific receptors. Recent advances in the field involving the generation of heteromer-specific reagents (antibodies or ligands) or of membrane-permeable peptides that disrupt the heteromer interaction are helping to elucidate the physiological role of opioid receptor heteromers and the contribution of the partner receptor to the side effects associated with opioid use. For example, studies using membrane-permeable peptides targeting the heteromer interface have implicated µ and δ receptor heteromers in the development of tolerance to morphine, and heteromers of µ and gastrin-releasing peptide receptors in morphine-induced itch. In addition, a number of ligands that selectively target opioid receptor heteromers exhibit potent antinociception with a decrease in the side effects commonly associated with morphine use. In this review, we summarize the latest findings regarding the biological and functional characteristics of opioid receptor heteromers both in vitro and in vivo.
[Mh] Termos MeSH primário: Receptores de Canabinoides/metabolismo
Receptores de Catecolaminas/metabolismo
Receptores Opioides/metabolismo
[Mh] Termos MeSH secundário: Animais
Desenho de Drogas
Seres Humanos
Multimerização Proteica
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Nm] Nome de substância:
0 (Receptors, Cannabinoid); 0 (Receptors, Catecholamine); 0 (Receptors, Opioid)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140612
[St] Status:MEDLINE
[do] DOI:10.1111/bph.12798


  8 / 205 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:24841610
[Au] Autor:Gibson JA; Raphael B
[Ad] Endereço:Jennifer A. Gibson is a nurse educator in the cardiac ICU at St. Paul's Hospital, Vancouver, B.C., Canada. Brooke Raphael is a staff nurse in the cardiac ICU at St. Paul's Hospital.
[Ti] Título:Understanding beta-blockers.
[So] Source:Nursing;44(6):55-9, 2014 Jun.
[Is] ISSN:1538-8689
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Antagonistas Adrenérgicos beta/farmacologia
Antagonistas Adrenérgicos beta/uso terapêutico
Sistema Nervoso Simpático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Síndrome Coronariana Aguda/tratamento farmacológico
Síndrome Coronariana Aguda/enfermagem
Antagonistas Adrenérgicos beta/efeitos adversos
Arritmias Cardíacas/tratamento farmacológico
Arritmias Cardíacas/enfermagem
Catecolaminas/farmacologia
Catecolaminas/uso terapêutico
Monitoramento de Medicamentos/enfermagem
Insuficiência Cardíaca/tratamento farmacológico
Insuficiência Cardíaca/enfermagem
Seres Humanos
Hipertensão/tratamento farmacológico
Hipertensão/enfermagem
Educação de Pacientes como Assunto
Receptores de Catecolaminas/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Catecholamines); 0 (Receptors, Catecholamine)
[Em] Mês de entrada:1412
[Cu] Atualização por classe:140520
[Lr] Data última revisão:
140520
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:140521
[St] Status:MEDLINE
[do] DOI:10.1097/01.NURSE.0000446633.63090.40


  9 / 205 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:24054152
[Au] Autor:Emery AC
[Ad] Endereço:Section on Molecular Neuroscience, Laboratory of Cellular and Molecular Regulation, National Institute of Mental Health Intramural Research Program, Bethesda, Maryland, USA. Electronic address: andrew.emery@nih.gov.
[Ti] Título:Catecholamine receptors: prototypes for GPCR-based drug discovery.
[So] Source:Adv Pharmacol;68:335-56, 2013.
[Is] ISSN:1557-8925
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Drugs acting at G protein-coupled receptors (GPCRs) constitute ~40% of those in current clinical use. GPCR-based drug discovery remains at the forefront of drug development, especially for new treatments for psychiatric illness and neurological disease. Here, the basic framework of GPCR signaling learned through the elucidation of catecholamine receptor signaling through G proteins and ß-arrestins, and X-ray crystallographic structure determination is reviewed. In silico docking studies developed in tandem with confirmatory empirical data gathering from binding and signaling experiments have allowed this basic framework to be expanded to drug hunting through predictive in silico searching as well as high-throughput and high-content screening approaches. For efforts moving forward for the deployment of new GPCR-acting drugs, collaborative efforts between industry and government/academic research in target validation at the molecular and cellular levels have become progressively more common. Polypharmacological approaches have become increasingly available for learning more about the mechanisms of GPCR-targeted drugs, based on interaction not with a single, but with a wide range of GPCR targets. These approaches are likely to aid in drug repurposing efforts, yield valuable insight on the side effects of currently employed drugs, and allow for a clearer picture of the actual targets of "atypical" drugs used in a variety of therapeutic contexts.
[Mh] Termos MeSH primário: Receptores de Catecolaminas/metabolismo
[Mh] Termos MeSH secundário: Animais
Descoberta de Drogas
Seres Humanos
Ligantes
Receptores Acoplados a Proteínas-G/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Ligands); 0 (Receptors, Catecholamine); 0 (Receptors, G-Protein-Coupled)
[Em] Mês de entrada:1405
[Cu] Atualização por classe:130923
[Lr] Data última revisão:
130923
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130924
[St] Status:MEDLINE


  10 / 205 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:23986246
[Au] Autor:Hapiak V; Summers P; Ortega A; Law WJ; Stein A; Komuniecki R
[Ad] Endereço:Department of Biological Sciences, University of Toledo, Toledo, Ohio 43606-3390, USA.
[Ti] Título:Neuropeptides amplify and focus the monoaminergic inhibition of nociception in Caenorhabditis elegans.
[So] Source:J Neurosci;33(35):14107-16, 2013 Aug 28.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Monoamines and neuropeptides interact to modulate most behaviors. To better understand these interactions, we have defined the roles of tyramine (TA), octopamine, and neuropeptides in the inhibition of aversive behavior in Caenorhabditis elegans. TA abolishes the serotonergic sensitization of aversive behavior mediated by the two nociceptive ASH sensory neurons and requires the expression of the adrenergic-like, Gαq-coupled, TA receptor TYRA-3 on inhibitory monoaminergic and peptidergic neurons. For example, TA inhibition requires Gαq and Gαs signaling in the peptidergic ASI sensory neurons, with an array of ASI neuropeptides activating neuropeptide receptors on additional neurons involved in locomotory decision-making. The ASI neuropeptides required for tyraminergic inhibition are distinct from those required for octopaminergic inhibition, suggesting that individual monoamines stimulate the release of different subsets of ASI neuropeptides. Together, these results demonstrate that a complex humoral mix of monoamines is focused by more local, synaptic, neuropeptide release to modulate nociception and highlight the similarities between the tyraminergic/octopaminergic inhibition of nociception in C. elegans and the noradrenergic inhibition of nociception in mammals that also involves inhibitory peptidergic signaling.
[Mh] Termos MeSH primário: Neuropeptídeos/metabolismo
Nociceptividade
Octopamina/farmacologia
Tiramina/farmacologia
[Mh] Termos MeSH secundário: Animais
Caenorhabditis elegans
Proteínas de Caenorhabditis elegans/antagonistas & inibidores
Proteínas de Caenorhabditis elegans/metabolismo
Subunidades alfa de Proteínas de Ligação ao GTP/metabolismo
Locomoção
Receptores de Catecolaminas/antagonistas & inibidores
Receptores de Catecolaminas/metabolismo
Células Receptoras Sensoriais/metabolismo
Células Receptoras Sensoriais/fisiologia
Transmissão Sináptica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (GTP-Binding Protein alpha Subunits); 0 (Neuropeptides); 0 (Receptors, Catecholamine); 0 (tyramine receptor 3, C elegans); 14O50WS8JD (Octopamine); X8ZC7V0OX3 (Tyramine)
[Em] Mês de entrada:1310
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130830
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1324-13.2013



página 1 de 21 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