Base de dados : MEDLINE
Pesquisa : D27.505.519.625.725 [Categoria DeCS]
Referências encontradas : 55 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 6 ir para página                

  1 / 55 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28174191
[Au] Autor:Belcik JT; Davidson BP; Xie A; Wu MD; Yadava M; Qi Y; Liang S; Chon CR; Ammi AY; Field J; Harmann L; Chilian WM; Linden J; Lindner JR
[Ad] Endereço:From Knight Cardiovascular Institute (J.T.B., B.P.D., A.X., M.Y., Y.Q., S.L., C.R.C., A.Y.A., J.R.L.), and Oregon National Primate Research Center (J.R.L.), Oregon Health & Science University, Portland; Doernbecher Children's Hospital, Portland, OR; Division of Hematology and Oncology, Medical C
[Ti] Título:Augmentation of Muscle Blood Flow by Ultrasound Cavitation Is Mediated by ATP and Purinergic Signaling.
[So] Source:Circulation;135(13):1240-1252, 2017 Mar 28.
[Is] ISSN:1524-4539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Augmentation of tissue blood flow by therapeutic ultrasound is thought to rely on convective shear. Microbubble contrast agents that undergo ultrasound-mediated cavitation markedly amplify these effects. We hypothesized that purinergic signaling is responsible for shear-dependent increases in muscle perfusion during therapeutic cavitation. METHODS: Unilateral exposure of the proximal hindlimb of mice (with or without ischemia produced by iliac ligation) to therapeutic ultrasound (1.3 MHz, mechanical index 1.3) was performed for 10 minutes after intravenous injection of 2×10 lipid microbubbles. Microvascular perfusion was evaluated by low-power contrast ultrasound perfusion imaging. In vivo muscle ATP release and in vitro ATP release from endothelial cells or erythrocytes were assessed by a luciferin-luciferase assay. Purinergic signaling pathways were assessed by studying interventions that (1) accelerated ATP degradation; (2) inhibited P2Y receptors, adenosine receptors, or K channels; or (3) inhibited downstream signaling pathways involving endothelial nitric oxide synthase or prostanoid production (indomethacin). Augmentation in muscle perfusion by ultrasound cavitation was assessed in a proof-of-concept clinical trial in 12 subjects with stable sickle cell disease. RESULTS: Therapeutic ultrasound cavitation increased muscle perfusion by 7-fold in normal mice, reversed tissue ischemia for up to 24 hours in the murine model of peripheral artery disease, and doubled muscle perfusion in patients with sickle cell disease. Augmentation in flow extended well beyond the region of ultrasound exposure. Ultrasound cavitation produced an ≈40-fold focal and sustained increase in ATP, the source of which included both endothelial cells and erythrocytes. Inhibitory studies indicated that ATP was a critical mediator of flow augmentation that acts primarily through either P2Y receptors or adenosine produced by ectonucleotidase activity. Combined indomethacin and inhibition of endothelial nitric oxide synthase abolished the effects of therapeutic ultrasound, indicating downstream signaling through both nitric oxide and prostaglandins. CONCLUSIONS: Therapeutic ultrasound using microbubble cavitation to increase muscle perfusion relies on shear-dependent increases in ATP, which can act through a diverse portfolio of purinergic signaling pathways. These events can reverse hindlimb ischemia in mice for >24 hours and increase muscle blood flow in patients with sickle cell disease. CLINICAL TRIAL REGISTRATION: URL: http://clinicaltrials.gov. Unique identifier: NCT01566890.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/metabolismo
Músculo Esquelético/irrigação sanguínea
Purinérgicos/metabolismo
Ultrassonografia/métodos
[Mh] Termos MeSH secundário: Animais
Hemodinâmica
Seres Humanos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Microbolhas
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Purinergic Agents); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170501
[Lr] Data última revisão:
170501
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCULATIONAHA.116.024826


  2 / 55 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27976523
[Au] Autor:Zhang PA; Xu QY; Xue L; Zheng H; Yan J; Xiao Y; Xu GY
[Ad] Endereço:Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Laboratory of Translational Pain Medicine, Institute of Neuroscience, Soochow University, Suzhou, China.
[Ti] Título:Neonatal Maternal Deprivation Enhances Presynaptic P2X7 Receptor Transmission in Insular Cortex in an Adult Rat Model of Visceral Hypersensitivity.
[So] Source:CNS Neurosci Ther;23(2):145-154, 2017 Feb.
[Is] ISSN:1755-5949
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:AIMS: Insular cortex (IC) is involved in processing the information of pain. The aim of this study was to investigate roles and mechanisms of P2X7 receptors (P2X7Rs) in IC in development of visceral hypersensitivity of adult rats with neonatal maternal deprivation (NMD). METHODS: Visceral hypersensitivity was quantified by abdominal withdrawal reflex threshold to colorectal distension (CRD). Expression of P2X7Rs was determined by qPCR and Western blot. Synaptic transmission in IC was recorded by patch-clamp recording. RESULTS: The expression of P2X7Rs and glutamatergic neurotransmission in IC was significantly increased in NMD rats when compared with age-matched controls. Application of BzATP (P2X7R agonist) enhanced the frequency of spontaneous excitatory postsynaptic currents (sEPSC) and miniature excitatory postsynaptic currents (mEPSC) in IC slices of control rats. Application of BBG (P2X7R antagonist) suppressed the frequencies of sEPSC and mEPSC in IC slices of NMD rats. Microinjection of BzATP into right IC significantly decreased CRD threshold in control rats while microinjection of BBG or A438079 into right IC greatly increased CRD threshold in NMD rats. CONCLUSION: Data suggested that the enhanced activities of P2X7Rs in IC, likely through a presynaptic mechanism, contributed to visceral hypersensitivity of adult rats with NMD.
[Mh] Termos MeSH primário: Córtex Cerebral/citologia
Privação Materna
Terminações Pré-Sinápticas/fisiologia
Receptores Purinérgicos P2X7/metabolismo
Dor Visceral/patologia
[Mh] Termos MeSH secundário: 2-Amino-5-fosfonovalerato/farmacologia
6-Ciano-7-nitroquinoxalina-2,3-diona/farmacologia
Trifosfato de Adenosina/análogos & derivados
Trifosfato de Adenosina/farmacologia
Animais
Animais Recém-Nascidos
Antagonistas de Aminoácidos Excitatórios/farmacologia
Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos
Técnicas In Vitro
Masculino
Fosfopiruvato Hidratase/metabolismo
Inibidores da Agregação de Plaquetas/farmacologia
Purinérgicos/farmacologia
Ratos
Ratos Sprague-Dawley
Sinaptofisina/metabolismo
Regulação para Cima/efeitos dos fármacos
Regulação para Cima/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Excitatory Amino Acid Antagonists); 0 (Platelet Aggregation Inhibitors); 0 (Purinergic Agents); 0 (Receptors, Purinergic P2X7); 0 (Synaptophysin); 4P5DXU1F8Q (3'-O-(4-benzoyl)benzoyladenosine 5'-triphosphate); 6OTE87SCCW (6-Cyano-7-nitroquinoxaline-2,3-dione); 76726-92-6 (2-Amino-5-phosphonovalerate); 8L70Q75FXE (Adenosine Triphosphate); EC 4.2.1.11 (Phosphopyruvate Hydratase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161216
[St] Status:MEDLINE
[do] DOI:10.1111/cns.12663


  3 / 55 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27927784
[Au] Autor:Agosto-Marlin IM; Nichols NL; Mitchell GS
[Ad] Endereço:Department of Comparative Biosciences, University of Wisconsin, Madison, Wisconsin; and.
[Ti] Título:Adenosine-dependent phrenic motor facilitation is inflammation resistant.
[So] Source:J Neurophysiol;117(2):836-845, 2017 Feb 01.
[Is] ISSN:1522-1598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Phrenic motor facilitation (pMF), a form of respiratory plasticity, can be elicited by acute intermittent hypoxia (i.e., phrenic long-term facilitation, pLTF) or direct application of drugs to the cervical spinal cord. Moderate acute intermittent hypoxia (mAIH; 3 × 5-min episodes of 35-50 mmHg arterial Po , 5-min normoxic intervals) induces pLTF by a serotonin-dependent mechanism; mAIH-induced pLTF is abolished by mild systemic inflammation induced by a low dose of lipopolysaccharide (LPS; 100 µg/kg ip). In contrast, severe acute intermittent hypoxia (sAIH; 3 × 5-min episodes of 25-30 mmHg arterial Po , 5-min normoxic intervals) elicits pLTF by a distinct, adenosine-dependent mechanism. Since it is not known if systemic LPS blocks the mechanism giving rise to sAIH-induced pLTF, we tested the hypothesis that sAIH-induced pLTF and adenosine 2A (A ) receptor-induced pMF are insensitive to mild systemic inflammation elicited by the same low dose of LPS. In agreement with our hypothesis, neither sAIH-induced pLTF nor cervical intrathecal A receptor agonist (CGS-21680; 200 µM, 10 µl × 3)-induced pMF were affected 24 h post-LPS. Pretreatment with intrathecal A receptor antagonist injections (MSX-3; 10 µM, 12 µl) blocked sAIH-induced pLTF 24 h post LPS, confirming that pLTF was adenosine dependent. Our results give insights concerning the differential impact of systemic inflammation and the functional significance of multiple cascades capable of giving rise to phrenic motor plasticity. The relative resistance of adenosine-dependent pMF to inflammation suggests that it provides a "backup" system in animals lacking serotonin-dependent pMF due to ongoing inflammation associated with systemic infections and/or neural injury. This study gives novel insights concerning how a mild systemic inflammation impacts phrenic motor plasticity (pMF), particularly adenosine-dependent pMF. We suggest that since this adenosine-dependent pathway is insensitive to systemic inflammation, it represents an alternative or "backup" mechanism of pMF when other mechanisms are suppressed.
[Mh] Termos MeSH primário: Adenosina/metabolismo
Potenciação de Longa Duração/fisiologia
Nervo Frênico/fisiologia
[Mh] Termos MeSH secundário: Adenosina/análogos & derivados
Adenosina/farmacologia
Análise de Variância
Animais
Glicemia/efeitos dos fármacos
Glicemia/fisiologia
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Hipóxia/complicações
Lipopolissacarídeos/toxicidade
Potenciação de Longa Duração/efeitos dos fármacos
Masculino
Fenetilaminas/farmacologia
Purinérgicos/farmacologia
Ratos
Ratos Sprague-Dawley
Síndrome de Resposta Inflamatória Sistêmica/induzido quimicamente
Síndrome de Resposta Inflamatória Sistêmica/etiologia
Fatores de Tempo
Xantinas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Lipopolysaccharides); 0 (MSX 3 compound); 0 (Phenethylamines); 0 (Purinergic Agents); 0 (Xanthines); 0 (lipid-linked oligosaccharides); 120225-54-9 (2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161209
[St] Status:MEDLINE
[do] DOI:10.1152/jn.00619.2016


  4 / 55 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27793264
[Au] Autor:Walton EL
[Ad] Endereço:Staff Writer at the Biomedical Journal, 56 Dronningens Gate, 7012 Trondheim, Norway. Electronic address: ewalton86@gmail.com.
[Ti] Título:Perturbing purinergic signaling: A pathogen's guidebook to counteracting inflammatory responses.
[So] Source:Biomed J;39(4):229-233, 2016 Aug.
[Is] ISSN:2320-2890
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this issue of the Biomedical Journal, we learn how bacteria and parasites alike counteract inflammatory signaling by manipulating purinergic signaling. We also focus on an original article shedding light on the role of an Epstein-Barr virus encoded gene in metastasis in nasopharyngeal carcinoma. Finally, we learn about a possible link between Trichomonas vaginalis and recurrent urinary tract infection.
[Mh] Termos MeSH primário: Leishmania/fisiologia
Porphyromonas/fisiologia
Purinérgicos
Trichomonas/fisiologia
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:EDITORIAL
[Nm] Nome de substância:
0 (Purinergic Agents)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161030
[St] Status:MEDLINE


  5 / 55 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27689756
[Au] Autor:Dziubina A; Szmyd K; Zygmunt M; Sapa J; Dudek M; Filipek B; Drabczynska A; Zaluski M; Pytka K; Kiec-Kononowicz K
[Ad] Endereço:Department of Pharmacodynamics, Jagiellonian University Medical College, Kraków, Poland. Electronic address: anna.dziubina@uj.edu.pl.
[Ti] Título:Evaluation of antidepressant-like and anxiolytic-like activity of purinedione-derivatives with affinity for adenosine A receptors in mice.
[So] Source:Pharmacol Rep;68(6):1285-1292, 2016 Dec.
[Is] ISSN:1734-1140
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: It has recently been suggested that the adenosine A receptor plays a role in several animal models of depression. Additionally, A antagonists have reversed behavioral deficits and exhibited a profile similar to classical antidepressants. METHODS: In the present study, imidazo- and pyrimido[2,1-f]purinedione derivatives (KD 66, KD 167, KD 206) with affinity to A receptors but poor A affinity were evaluated for their antidepressant- and anxiolytic-like activity. The activity of these derivatives was tested using a tail suspension and forced swim test, two widely-used behavioral paradigms for the evaluation of antidepressant-like activity. In turn, the anxiolytic activity was evaluated using the four-plate test. RESULTS: The results showed the antidepressant-like activity of pyrimido- and imidazopurinedione derivatives (i.e. KD 66, KD 167 and KD 206) in acute and chronic behavioral tests in mice. KD 66 revealed an anxiolytic-like effect, while KD 167 increased anxiety behaviors. KD 206 had no effect on anxiety. Furthermore, none of the tested compounds increased locomotor activity. CONCLUSION: Available data support the proposition that the examined compounds with adenosine A receptor affinity may be an interesting target for the development of antidepressant and/or anxiolytic agents.
[Mh] Termos MeSH primário: Ansiolíticos/metabolismo
Ansiolíticos/uso terapêutico
Antidepressivos/metabolismo
Antidepressivos/uso terapêutico
Purinérgicos/metabolismo
Purinérgicos/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Ansiolíticos/química
Antidepressivos/química
Ansiedade/tratamento farmacológico
Ansiedade/metabolismo
Ansiedade/psicologia
Depressão/tratamento farmacológico
Depressão/metabolismo
Depressão/psicologia
Relação Dose-Resposta a Droga
Avaliação Pré-Clínica de Medicamentos/métodos
Imobilização/métodos
Imobilização/psicologia
Masculino
Camundongos
Purinérgicos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Anxiety Agents); 0 (Antidepressive Agents); 0 (Purinergic Agents)
[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:161001
[St] Status:MEDLINE


  6 / 55 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27574293
[Au] Autor:Fleck D; Mundt N; Bruentgens F; Geilenkirchen P; Machado PA; Veitinger T; Veitinger S; Lipartowski SM; Engelhardt CH; Oldiges M; Spehr J; Spehr M
[Ad] Endereço:Department of Chemosensation, Institute for Biology II, RWTH Aachen University, D-52074 Aachen, Germany.
[Ti] Título:Distinct purinergic signaling pathways in prepubescent mouse spermatogonia.
[So] Source:J Gen Physiol;148(3):253-71, 2016 09.
[Is] ISSN:1540-7748
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Spermatogenesis ranks among the most complex, yet least understood, developmental processes. The physiological principles that control male germ cell development in mammals are notoriously difficult to unravel, given the intricate anatomy and complex endo- and paracrinology of the testis. Accordingly, we lack a conceptual understanding of the basic signaling mechanisms within the testis, which control the seminiferous epithelial cycle and thus govern spermatogenesis. Here, we address paracrine signal transduction in undifferentiated male germ cells from an electrophysiological perspective. We identify distinct purinergic signaling pathways in prepubescent mouse spermatogonia, both in vitro and in situ. ATP-a dynamic, widespread, and evolutionary conserved mediator of cell to cell communication in various developmental contexts-activates at least two different spermatogonial purinoceptor isoforms. Both receptors operate within nonoverlapping stimulus concentration ranges, display distinct response kinetics and, in the juvenile seminiferous cord, are uniquely expressed in spermatogonia. We further find that spermatogonia express Ca(2+)-activated large-conductance K(+) channels that appear to function as a safeguard against prolonged ATP-dependent depolarization. Quantitative purine measurements additionally suggest testicular ATP-induced ATP release, a mechanism that could increase the paracrine radius of initially localized signaling events. Moreover, we establish a novel seminiferous tubule slice preparation that allows targeted electrophysiological recordings from identified testicular cell types in an intact epithelial environment. This unique approach not only confirms our in vitro findings, but also supports the notion of purinergic signaling during the early stages of spermatogenesis.
[Mh] Termos MeSH primário: Purinérgicos/metabolismo
Transdução de Sinais/fisiologia
Espermatogônias/metabolismo
Espermatogônias/fisiologia
[Mh] Termos MeSH secundário: Trifosfato de Adenosina/metabolismo
Animais
Comunicação Celular/fisiologia
Células Epiteliais/metabolismo
Células Epiteliais/fisiologia
Feminino
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Canais de Potássio Cálcio-Ativados/metabolismo
Túbulos Seminíferos/metabolismo
Túbulos Seminíferos/fisiologia
Espermatogênese/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Potassium Channels, Calcium-Activated); 0 (Purinergic Agents); 8L70Q75FXE (Adenosine Triphosphate)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160831
[St] Status:MEDLINE
[do] DOI:10.1085/jgp.201611636


  7 / 55 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27442785
[Au] Autor:Back MJ; Lee HK; Lee JH; Fu Z; Son MW; Choi SZ; Go HS; Yoo S; Hwang SW; Kim DK
[Ad] Endereço:Department of Environmental and Health Chemistry, College of Pharmacy, Chung-Ang University ; 84 Heukseok-ro, Dongjak-Ku, Seoul 06974, Republic of Korea.
[Ti] Título:P2X1 Receptor-Mediated Ca Influx Triggered by DA-9801 Potentiates Nerve Growth Factor-Induced Neurite Outgrowth.
[So] Source:ACS Chem Neurosci;7(11):1488-1498, 2016 Nov 16.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nerve growth factor (NGF)-induced neuronal regeneration has emerged as a strategy to treat neuronal degeneration-associated disorders. However, direct NGF administration is limited by the occurrence of adverse effects at high doses of NGF. Therefore, development of a therapeutic strategy to promote the NGF trophic effect is required. In view of the lack of understanding of the mechanism for potentiating the NGF effect, this study investigated molecular targets of DA-9801, a well-standardized Dioscorea rhizome extract, which has a promoting effect on NGF. An increase in intracellular calcium ion level was induced by DA-9801, and chelation of extracellular calcium ions with ethylene-bis(oxyethylenenitrilo)tetraacetic acid (EGTA) suppressed the potentiating effect of DA-9801 on NGF-induced neurite outgrowth. In addition, EGTA treatment reduced the DA-9801-induced phosphorylation of extracellular signal-regulated kinase1/2 (ERK1/2), the major mediators of neurite outgrowth. To find which calcium ion-permeable channel contributes to the calcium ion influx induced by DA-9801, we treated PC12 cells with various inhibitors of calcium ion-permeable channels. NF449, a P2X1 receptor selective antagonist, significantly abolished the potentiating effect of DA-9801 on NGF-induced neurite outgrowth and abrogated the DA-9801-induced ERK1/2 phosphorylation. In addition, transfection with siRNA of P2X1 receptor significantly reduced the DA-9801-enhanced neurite outgrowth. In conclusion, calcium ion influx through P2X1 receptor mediated the promoting effect of DA-9801 on NGF-induced neurite outgrowth via ERK1/2 phosphorylation.
[Mh] Termos MeSH primário: Fator de Crescimento Neural/metabolismo
Neuritos/efeitos dos fármacos
Crescimento Neuronal/efeitos dos fármacos
Preparações de Plantas/farmacologia
Purinérgicos/farmacologia
Receptores Purinérgicos P2X1/metabolismo
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Quelantes de Cálcio/farmacologia
Cátions Bivalentes/metabolismo
Ácido Egtázico/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Sistema de Sinalização das MAP Quinases/fisiologia
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Neuritos/fisiologia
Crescimento Neuronal/fisiologia
Fármacos Neuroprotetores/farmacologia
Células PC12
Fosforilação/efeitos dos fármacos
RNA Interferente Pequeno
Ratos
Receptores Purinérgicos P2X1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Chelating Agents); 0 (Cations, Divalent); 0 (DA-9801); 0 (Neuroprotective Agents); 0 (Plant Preparations); 0 (Purinergic Agents); 0 (RNA, Small Interfering); 0 (Receptors, Purinergic P2X1); 526U7A2651 (Egtazic Acid); 9061-61-4 (Nerve Growth Factor); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170621
[Lr] Data última revisão:
170621
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160722
[St] Status:MEDLINE


  8 / 55 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:27100625
[Au] Autor:Rahbar S; Pan W; Jonz MG
[Ad] Endereço:Department of Biology, University of Ottawa, Ottawa, Ontario, Canada.
[Ti] Título:Purinergic and Cholinergic Drugs Mediate Hyperventilation in Zebrafish: Evidence from a Novel Chemical Screen.
[So] Source:PLoS One;11(4):e0154261, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A rapid test to identify drugs that affect autonomic responses to hypoxia holds therapeutic and ecologic value. The zebrafish (Danio rerio) is a convenient animal model for investigating peripheral O2 chemoreceptors and respiratory reflexes in vertebrates; however, the neurotransmitters and receptors involved in this process are not adequately defined. The goals of the present study were to demonstrate purinergic and cholinergic control of the hyperventilatory response to hypoxia in zebrafish, and to develop a procedure for screening of neurochemicals that affect respiration. Zebrafish larvae were screened in multi-well plates for sensitivity to the cholinergic receptor agonist, nicotine, and antagonist, atropine; and to the purinergic receptor antagonists, suramin and A-317491. Nicotine increased ventilation frequency (fV) maximally at 100 µM (EC50 = 24.5 µM). Hypoxia elevated fV from 93.8 to 145.3 breaths min-1. Atropine reduced the hypoxic response only at 100 µM. Suramin and A-317491 maximally reduced fV at 50 µM (EC50 = 30.4 and 10.8 µM) and abolished the hyperventilatory response to hypoxia. Purinergic P2X3 receptors were identified in neurons and O2-chemosensory neuroepithelial cells of the gills using immunohistochemistry and confocal microscopy. These studies suggest a role for purinergic and nicotinic receptors in O2 sensing in fish and implicate ATP and acetylcholine in excitatory neurotransmission, as in the mammalian carotid body. We demonstrate a rapid approach for screening neuroactive chemicals in zebrafish with implications for respiratory medicine and carotid body disease in humans; as well as for preservation of aquatic ecosystems.
[Mh] Termos MeSH primário: Colinérgicos/farmacologia
Purinérgicos/farmacologia
Respiração/efeitos dos fármacos
Peixe-Zebra/fisiologia
[Mh] Termos MeSH secundário: Animais
Atropina/farmacologia
Feminino
Brânquias/efeitos dos fármacos
Brânquias/metabolismo
Hiperventilação/fisiopatologia
Hipóxia
Imuno-Histoquímica
Larva/efeitos dos fármacos
Larva/metabolismo
Larva/fisiologia
Masculino
Microscopia Confocal
Antagonistas Muscarínicos/farmacologia
Nicotina/farmacologia
Agonistas Nicotínicos/farmacologia
Fenóis/farmacologia
Compostos Policíclicos/farmacologia
Receptores Nicotínicos/metabolismo
Receptores Purinérgicos P2X3/metabolismo
Suramina/farmacologia
Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (A-317491); 0 (Cholinergic Agents); 0 (Muscarinic Antagonists); 0 (Nicotinic Agonists); 0 (Phenols); 0 (Polycyclic Compounds); 0 (Purinergic Agents); 0 (Receptors, Nicotinic); 0 (Receptors, Purinergic P2X3); 6032D45BEM (Suramin); 6M3C89ZY6R (Nicotine); 7C0697DR9I (Atropine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170405
[Lr] Data última revisão:
170405
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160422
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0154261


  9 / 55 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27087530
[Au] Autor:Klaft ZJ; Hollnagel JO; Salar S; Caliskan G; Schulz SB; Schneider UC; Horn P; Koch A; Holtkamp M; Gabriel S; Gerevich Z; Heinemann U
[Ad] Endereço:Institute of Neurophysiology, Charité - Universitätsmedizin Berlin, Berlin, Germany.
[Ti] Título:Adenosine A1 receptor-mediated suppression of carbamazepine-resistant seizure-like events in human neocortical slices.
[So] Source:Epilepsia;57(5):746-56, 2016 May.
[Is] ISSN:1528-1167
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The need for alternative pharmacologic strategies in treatment of epilepsies is pressing for about 30% of patients with epilepsy who do not experience satisfactory seizure control with present treatments. In temporal lobe epilepsy (TLE) even up to 80% of patients are pharmacoresistant, and surgical resection of the ictogenic tissue is only possible for a minority of TLE patients. In this study we investigate purinergic modulation of drug-resistant seizure-like events (SLEs) in human temporal cortex slices. METHODS: Layer V/VI field potentials from a total of 77 neocortical slices from 17 pharmacoresistant patients were recorded to monitor SLEs induced by application of 8 mM [K(+) ] and 50 µm bicuculline. RESULTS: Activating A1 receptors with a specific agonist completely suppressed SLEs in 73% of human temporal cortex slices. In the remaining slices, incidence of SLEs was markedly reduced. Because a subportion of slices can be pharmacosensitive, we tested effects of an A1 agonist, in slices insensitive to a high dose of carbamazepine (50 µm). Also in these cases the A1 agonist was equally efficient. Moreover, ATP and adenosine blocked or modulated SLEs, an effect mediated not by P2 receptors but rather by adenosine A1 receptors. SIGNIFICANCE: Selective activation of A1 receptors mediates a strong anticonvulsant action in human neocortical slices from pharmacoresistant patients. We propose that our human slice model of seizure-like activity is a feasible option for future studies investigating new antiepileptic drug (AED) candidates.
[Mh] Termos MeSH primário: Epilepsia Resistente a Medicamentos/patologia
Neocórtex/efeitos dos fármacos
Neocórtex/metabolismo
Receptores Purinérgicos P1/metabolismo
[Mh] Termos MeSH secundário: Adenosina/análogos & derivados
Adenosina/farmacologia
Trifosfato de Adenosina/farmacologia
Adulto
Bicuculina/análogos & derivados
Bicuculina/farmacologia
Carbamazepina/efeitos adversos
Carbamazepina/farmacologia
Epilepsia Resistente a Medicamentos/tratamento farmacológico
Estimulação Elétrica
Potenciais Evocados/efeitos dos fármacos
Feminino
Seres Humanos
Técnicas In Vitro
Masculino
Meia-Idade
Potássio/farmacologia
Purinérgicos/farmacologia
Fatores de Tempo
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Purinergic Agents); 0 (Receptors, Purinergic P1); 130714-47-5 (N(6)-cyclohexyl-2-O-methyladenosine); 33CM23913M (Carbamazepine); 40709-69-1 (bicuculline methiodide); 8L70Q75FXE (Adenosine Triphosphate); K72T3FS567 (Adenosine); RWP5GA015D (Potassium); Y37615DVKC (Bicuculline)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170531
[Lr] Data última revisão:
170531
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160419
[St] Status:MEDLINE
[do] DOI:10.1111/epi.13360


  10 / 55 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27002391
[Au] Autor:Akinyemi AJ; Thomé GR; Morsch VM; Bottari NB; Baldissarelli J; de Oliveira LS; Goularte JF; Belló-Klein A; Duarte T; Duarte M; Boligon AA; Athayde ML; Akindahunsi AA; Oboh G; Schetinger MR
[Ad] Endereço:Functional Foods and Nutraceuticals Unit, Department of Biochemistry, Federal University of Technology, Akure, Nigeria.
[Ti] Título:Effect of Ginger and Turmeric Rhizomes on Inflammatory Cytokines Levels and Enzyme Activities of Cholinergic and Purinergic Systems in Hypertensive Rats.
[So] Source:Planta Med;82(7):612-20, 2016 May.
[Is] ISSN:1439-0221
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Inflammation exerts a crucial pathogenic role in the development of hypertension. Hence, the aim of the present study was to investigate the effects of ginger (Zingiber officinale) and turmeric (Curcuma longa) on enzyme activities of purinergic and cholinergic systems as well as inflammatory cytokine levels in Nω-nitro-L-arginine methyl ester hydrochloride-induced hypertensive rats. The rats were divided into seven groups (n = 10); groups 1-3 included normotensive control rats, hypertensive (Nω-nitro-L-arginine methyl ester hydrochloride) rats, and hypertensive control rats treated with atenolol (an antihypertensive drug), while groups 4 and 5 included normotensive and hypertensive (Nω-nitro-L-arginine methyl ester hydrochloride) rats treated with 4 % supplementation of turmeric, respectively, and groups 6 and 7 included normotensive and hypertensive rats treated with 4 % supplementation of ginger, respectively. The animals were induced with hypertension by oral administration of Nω-nitro-L-arginine methyl ester hydrochloride, 40 mg/kg body weight. The results revealed a significant increase in ATP and ADP hydrolysis, adenosine deaminase, and acetylcholinesterase activities in lymphocytes from Nω-nitro-L-arginine methyl ester hydrochloride hypertensive rats when compared with the control rats. In addition, an increase in serum butyrylcholinesterase activity and proinflammatory cytokines (interleukin-1 and - 6, interferon-γ, and tumor necrosis factor-α) with a concomitant decrease in anti-inflammatory cytokines (interleukin-10) was observed in Nω-nitro-L-arginine methyl ester hydrochloride hypertensive rats. However, dietary supplementation of both rhizomes was efficient in preventing these alterations in hypertensive rats by decreasing ATP hydrolysis, acetylcholinesterase, and butyrylcholinesterase activities and proinflammatory cytokines in hypertensive rats. Thus, these activities could suggest a possible insight about the protective mechanisms of the rhizomes against hypertension-related inflammation.
[Mh] Termos MeSH primário: Acetilcolinesterase/metabolismo
Butirilcolinesterase/metabolismo
Curcuma
Citocinas/metabolismo
Gengibre
Hipertensão/dietoterapia
Preparações de Plantas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Colinérgicos/isolamento & purificação
Colinérgicos/farmacologia
Hipertensão/enzimologia
Masculino
Purinérgicos/isolamento & purificação
Purinérgicos/farmacologia
Ratos
Ratos Wistar
Rizoma
Linfócitos T/efeitos dos fármacos
Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cholinergic Agents); 0 (Cytokines); 0 (Plant Preparations); 0 (Purinergic Agents); EC 3.1.1.7 (Acetylcholinesterase); EC 3.1.1.8 (Butyrylcholinesterase)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160323
[St] Status:MEDLINE
[do] DOI:10.1055/s-0042-102062



página 1 de 6 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