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Id: lil-796033
Autor: Andrade, Daniela Medeiros Lobo de; Borges, Leonardo Luis; Torres, Ieda Maria Sapateiro; Conceição, Edemilson Cardoso da; Rocha, Matheus Lavorenti.
Título: Jabuticaba-Induced Endothelium-Independent Vasodilating Effect on Isolated Arteries / Efeito Vasodilatador Independente do Endotélio Induzido pela Jabuticaba (M. cauliflora) em Artérias Isoladas
Fonte: Arq. bras. cardiol;107(3):223-229, Sept. 2016. graf.
Idioma: en.
Projeto: Goiás State Research Support Foundation.
Resumo: Abstract Background: Despite the important biological effects of jabuticaba, its actions on the cardiovascular system have not been clarified. Objectives: To determine the effects of jabuticaba hydroalcoholic extract (JHE) on vascular smooth muscle (VSM) of isolated arteries. Methods: Endothelium-denuded aortic rings of rats were mounted in isolated organ bath to record isometric tension. The relaxant effect of JHE and the influence of K+ channels and Ca2+ intra- and extracellular sources on JHE-stimulated response were assessed. Results: Arteries pre-contracted with phenylephrine showed concentration-dependent relaxation (0.380 to 1.92 mg/mL). Treatment with K+ channel blockers (tetraethyl-ammonium, glibenclamide, 4-aminopyridine) hindered relaxation due to JHE. In addition, phenylephrine-stimulated contraction was hindered by previous treatment with JHE. Inhibition of sarcoplasmic reticulum Ca2+ ATPase did not change relaxation due to JHE. In addition, JHE inhibited the contraction caused by Ca2+ influx stimulated by phenylephrine and KCl (75 mM). Conclusion: JHE induces endothelium-independent vasodilation. Activation of K+ channels and inhibition of Ca2+ influx through the membrane are involved in the JHE relaxant effect.

Resumo Fundamentos: Embora a jabuticaba apresente importantes efeitos biológicos, suas ações sobre o sistema cardiovascular ainda não foram esclarecidas. Objetivos: Determinar os efeitos do extrato de jabuticaba (EHJ) sobre o músculo liso vascular (MLV) em artérias isoladas. Métodos: Aortas (sem endotélio) de ratos foram montadas em banho de órgãos isolados para registro de tensão isométrica. Foram verificados o efeito relaxante, a influência dos canais de K+ e das fontes de Ca2+ intra- e extracelular sob a resposta estimulada pelo EHJ. Resultados: Artérias pré-contraídas com fenilefrina apresentaram relaxamento concentração-dependente (0,380 a 1,92 mg/mL). O tratamento com bloqueadores de canais de K+ (tetraetilamônio, glibenclamida, 4-aminopiridina) prejudicaram o relaxamento pelo EHJ. A contração estimulada com fenilefrina também foi prejudicada pelo tratamento prévio com EHJ. A inibição da Ca2+ATPase do reticulo sarcoplasmático não alterou o relaxamento pelo EHJ. Além disso, o EHJ inibiu a contração causada pelo influxo de Ca2+ estimulado por fenilefrina e KCl (75 mM). Conclusão: O EHJ induz vasodilatação independente do endotélio. Ativação dos canais de K+ e inibição do influxo de Ca2+ através da membrana estão envolvidas no efeito relaxante do EHJ.
Descritores: Vasodilatadores/farmacologia
Extratos Vegetais/farmacologia
Myrtaceae/química
Músculo Liso Vascular/efeitos dos fármacos
-Aorta Torácica/efeitos dos fármacos
Fatores de Tempo
Vasoconstrição/efeitos dos fármacos
Vasodilatação/efeitos dos fármacos
Bloqueadores dos Canais de Cálcio/farmacologia
Verapamil/farmacologia
Canais de Cálcio/efeitos dos fármacos
Canais de Potássio/efeitos dos fármacos
Membrana Celular/efeitos dos fármacos
Reprodutibilidade dos Testes
Ratos Wistar
Bloqueadores dos Canais de Potássio/farmacologia
Limites: Animais
Masculino
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME


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Id: biblio-1147979
Autor: Ballón Paucara, Wendy Guadalupe; Grados-Torrez, Ricardo Enrique.
Título: Dinámica estructural entre la conformación abierta y cerrada del canal KATP en células pancreáticas / Structural dynamics between the open and closed conformations of the KATP channel in pancreatic cells
Fonte: Con-ciencia (La Paz);8(2):21-34, 2020. ilus..
Idioma: en.
Resumo: INTRODUCCIÓN: el canal de Potasio sensible a ATP (canal KATP) regula la producción de Insulina por células ß pancreáticas. La Glibenclamida (GBM) (fármaco antidiabético) y el ATP actúan como inhibidores de este canal, mientras que el ADP lo activa. El canal KATP es un octámero constituido por 4 subunidades centrales Kir6.2 que forman el poro y 4 subunidades externas de regulación SUR1. OBJETIVO: determinar la dinámica estructural entre las conformaciones abierta y cerrada del canal KATP en células pancreáticas. MÉTODO: análisis estructural comparativo de diferentes estructuras cristalográficas del canal KATP de células pancreáticas humanas empleando el software Chimera v1.11.2 RESULTADOS: La subunidad Kir6.2 presenta un dominio de unión a PIP2 (activador), una Hélice Interfacial (IFH) y un dominio N-terminal (KNtp). Por otro lado, la subunidad SUR1 que contiene el sitio de unión a la GBM, tiene 2 Dominios de Unión a Nucleótidos (NBD1/2), un bucle M5-Lh1 y un Motivo de Lazo formado por la interface entre el Dominio Trans-membrana 0 y el Bucle 0 (TMD0-L0). Los resultados del análisis dinámico estructural mediante herramientas bioinformáticas, indican que estas regiones participan activamente en los cambios conformacionales que dan lugar al cierre (inhibición) o apertura (activación) de este canal. CONCLUSIÓN: El estudio de la dinámica de activación e inhibición de los canales KATP es imprescindible para la evaluación, descubrimiento y/o diseño de nuevos compuestos naturales, que como la GBM, puedan promover la secreción de Insulina para coadyuvar o mejorar el tratamiento de pacientes diabéticos.

INTRODUCTION: the ATP-sensitive Potassium channel (KATP channel) regulates insulin production by pancreatic ß cells. Glibenclamide (GBM) (antidiabetic drug) and ATP act as inhibitors of this channel, while ADP activates it. The KATP channel is an octamer consisting of 4 central Kir6.2 subunits that form the pore and 4 external regulation subunits SUR1. OBJECTIVE: to determine the structural dynamics between the open and closed conformations of the KATP channel in pancreatic cells. METHOD: comparative structural analysis of different crystallographic structures of the KATP channel of human pancreatic cells using Chimera v1.11.2. RESULTS: the Kir6.2 subunit has a PIP2 binding domain (activator), an Interfacial Helix (IFH) and an N-terminal domain (KNtp). On the other hand, the SUR1 subunit that contains the GBM binding site, has 2 Nucleotide Binding Domains (NBD1/2), an M5-Lh1 loop and a Lasso Motif formed by the interface between the Trans-membrane Domain 0 and Loop 0 (TMD0-L0). The results of the dynamic structural analysis using bioinformatics tools indicate that these regions participate actively in the conformational changes that lead to the closure (inhibition) or opening (activation) of this channel. CONCLUSION: the study of the dynamics of activation and inhibition of the KATP channels is essential for the evaluation, discovery and/or design of new natural compounds, which like GBM, can promote insulin secretion to aid or improve the treatment of diabetic patients.
Descritores: Software
Canais de Potássio
Difosfato de Adenosina
-Pacientes
Insulina
Limites: Humanos
Responsável: BO138.1 - Biblioteca Central


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Id: biblio-888990
Autor: Lozano-Cuenca, J; González-Hernández, A; López-Canales, OA; Villagrana-Zesati, JR; Rodríguez-Choreão, JD; Morín-Zaragoza, R; Castillo-Henkel, EF; López-Canales, JS.
Título: Possible mechanisms involved in the vasorelaxant effect produced by clobenzorex in aortic segments of rats
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;50(9):e5765, 2017. tab, graf.
Idioma: en.
Resumo: Clobenzorex is a metabolic precursor of amphetamine indicated for the treatment of obesity. Amphetamines have been involved with cardiovascular side effects such as hypertension and pulmonary arterial hypertension. The aim of the present study was to investigate whether the direct application of 10-9-10-5 M clobenzorex on isolated phenylephrine-precontracted rat aortic rings produces vascular effects, and if so, what mechanisms may be involved. Clobenzorex produced an immediate concentration-dependent vasorelaxant effect at the higher concentrations (10-7.5-10-5 M). The present outcome was not modified by 10-6 M atropine (an antagonist of muscarinic acetylcholine receptors), 3.1×10-7 M glibenclamide (an ATP-sensitive K+ channel blocker), 10-3 M 4-aminopyridine (4-AP; a voltage-activated K+ channel blocker), 10-5 M indomethacin (a prostaglandin synthesis inhibitor), 10-5 M clotrimazole (a cytochrome P450 inhibitor) or 10-5 M cycloheximide (a general protein synthesis inhibitor). Contrarily, the clobenzorex-induced vasorelaxation was significantly attenuated (P<0.05) by 10-5 M L-NAME (a direct inhibitor of nitric oxide synthase), 10-7 M ODQ (an inhibitor of nitric oxide-sensitive guanylyl cyclase), 10-6 M KT 5823 (an inhibitor of protein kinase G), 10-2 M TEA (a Ca2+-activated K+ channel blocker and non-specific voltage-activated K+ channel blocker) and 10-7 M apamin plus 10-7 M charybdotoxin (blockers of small- and large-conductance Ca2+-activated K+ channels, respectively), and was blocked by 8×10-2 M potassium (a high concentration) and removal of the vascular endothelium. These results suggest that the direct vasorelaxant effect by clobenzorex on phenylephrine-precontracted rat aortic rings involved stimulation of the NO/cGMP/PKG/Ca2+-activated K+ channel pathway.
Descritores: Anfetaminas/farmacologia
Aorta Torácica/efeitos dos fármacos
Endotélio Vascular/efeitos dos fármacos
Vasodilatação
Vasodilatadores/farmacologia
-Canais de Cálcio/efeitos dos fármacos
Canais de Cálcio/metabolismo
Óxido Nítrico Sintase Tipo III/efeitos dos fármacos
Óxido Nítrico Sintase Tipo III/metabolismo
Canais de Potássio de Abertura Dependente da Tensão da Membrana/efeitos dos fármacos
Canais de Potássio de Abertura Dependente da Tensão da Membrana/metabolismo
Canais de Potássio/efeitos dos fármacos
Canais de Potássio/metabolismo
Ratos Wistar
Limites: Animais
Masculino
Ratos
Responsável: BR1.1 - BIREME


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Id: lil-769752
Autor: Baldev, N.; Sriram, R.; Prabu, P.C.; Gino, A. Kurian.
Título: Effect of mitochondrial potassium channel on the renal protection mediated by sodium thiosulfate against ethylene glycol induced nephrolithiasis in rat model
Fonte: Int. braz. j. urol;41(6):1116-1125, Nov.-Dec. 2015. tab, graf.
Idioma: en.
Resumo: Purpose: Sodium thiosulfate (STS) is clinically reported to be a promising drug in preventing nephrolithiasis. However, its mechanism of action remains unclear. In the present study, we investigated the role of mitochondrial KATP channel in the renal protection mediated by STS. Materials and Methods: Nephrolithiasis was induced in Wistar rats by administrating 0.4% ethylene glycol (EG) along with 1% ammonium chloride for one week in drinking water followed by only 0.75% EG for two weeks. Treatment groups received STS, mitochondrial KATP channel opener and closer exclusively or in combination with STS for two weeks. Results: Animals treated with STS showed normal renal tissue architecture, supported by near normal serum creatinine, urea and ALP activity. Diazoxide (mitochondria KATP channel opening) treatment to the animal also showed normal renal tissue histology and improved serum chemistry. However, an opposite result was shown by glibenclamide (mitochondria KATP channel closer) treated rats. STS administered along with diazoxide negated the renal protection rendered by diazoxide alone, while it imparted protection to the glibenclamide treated rats, formulating a mitochondria modulated STS action. Conclusion: The present study confirmed that STS render renal protection not only through chelation and antioxidant effect but also by modulating the mitochondrial KATP channel for preventing urolithiasis.
Descritores: Antioxidantes/farmacocinética
Quelantes/farmacologia
Etilenoglicol
Nefrolitíase/prevenção & controle
Canais de Potássio/farmacologia
Tiossulfatos/farmacologia
-Antioxidantes/uso terapêutico
Oxalato de Cálcio/metabolismo
Quelantes/uso terapêutico
Modelos Animais de Doenças
Eletroforese em Gel de Ágar
Rim/efeitos dos fármacos
Rim/patologia
Peroxidação de Lipídeos/efeitos dos fármacos
Nefrolitíase/patologia
Canais de Potássio/uso terapêutico
Distribuição Aleatória
Ratos Wistar
Reprodutibilidade dos Testes
Resultado do Tratamento
Tiossulfatos/uso terapêutico
Limites: Animais
Masculino
Responsável: BR1.1 - BIREME


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Id: lil-748220
Autor: Wang, C.; Hu, S.M.; Xie, H.; Qiao, S.G.; Liu, H.; Liu, C.F..
Título: Role of mitochondrial ATP-sensitive potassium channel-mediated PKC-ε in delayed protection against myocardial ischemia/reperfusion injury in isolated hearts of sevoflurane-preconditioned rats
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;48(6):528-536, 06/2015. tab, graf.
Idioma: en.
Projeto: the Natural Science Foundation of Jiangsu Province; . the Technology Bureau of Suzhou, China.
Resumo: This study aimed to determine the role of mitochondrial adenosine triphosphate-sensitive potassium (mitoKATP) channels and protein kinase C (PKC)-ε in the delayed protective effects of sevoflurane preconditioning using Langendorff isolated heart perfusion models. Fifty-four isolated perfused rat hearts were randomly divided into 6 groups (n=9). The rats were exposed for 60 min to 2.5% sevoflurane (the second window of protection group, SWOP group) or 33% oxygen inhalation (I/R group) 24 h before coronary occlusion. The control group (CON) and the sevoflurane group (SEVO) group were exposed to 33% oxygen and 2.5% sevoflurane for 60 min, respectively, without coronary occlusion. The mitoKATP channel inhibitor 5-hydroxydecanoate (5-HD) was given 30 min before sevoflurane preconditioning (5-HD+SWOP group). Cardiac function indices, infarct sizes, serum cardiac troponin I (cTnI) concentrations, and the expression levels of phosphorylated PKC-ε (p-PKC-ε) and caspase-8 were measured. Cardiac function was unchanged, p-PKC-ε expression was upregulated, caspase-8 expression was downregulated, cTnI concentrations were decreased, and the infarcts were significantly smaller (P<0.05) in the SWOP group compared with the I/R group. Cardiac function was worse, p-PKC-ε expression was downregulated, caspase-8 expression was upregulated, cTnI concentration was increased and infarcts were larger in the 5-HD+SWOP group (P<0.05) compared with the SWOP group. The results suggest that mitoKATP channels are involved in the myocardial protective effects of sevoflurane in preconditioning against I/R injury, by regulating PKC-ε phosphorylation before ischemia, and by downregulating caspase-8 during reperfusion.
Descritores: Precondicionamento Isquêmico Miocárdico/métodos
Éteres Metílicos/farmacologia
Traumatismo por Reperfusão Miocárdica/prevenção & controle
Inibidores da Agregação de Plaquetas/farmacologia
Canais de Potássio/farmacologia
Proteína Quinase C/farmacologia
-Antiarrítmicos/farmacologia
Western Blotting
/análise
CASPASE ABDOMINAL NEOPLASMS/análise
Ácidos Decanoicos/farmacologia
Coração/efeitos dos fármacos
Coração/fisiopatologia
Hemodinâmica/efeitos dos fármacos
Hidroxiácidos/farmacologia
Isquemia/prevenção & controle
Substâncias Protetoras/farmacologia
Distribuição Aleatória
Ratos Sprague-Dawley
Reprodutibilidade dos Testes
Fatores de Tempo
Troponina I/análise
Limites: Animais
Masculino
Tipo de Publ: Estudo de Avaliação
Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-748218
Autor: López-Canales, J.S.; Lozano-Cuenca, J.; Muãoz-Islas, E.; Aguilar-Carrasco, J.C.; López-Canales, O.A.; López-Mayorga, R.M.; Castillo-Henkel, E.F.; Valencia-Hernández, I.; Castillo-Henkel, C..
Título: Mechanisms involved in the vasorelaxant effects produced by the acute application of amfepramone in vitro to rat aortic rings
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;48(6):537-544, 06/2015. graf.
Idioma: en.
Resumo: Amfepramone (diethylpropion) is an appetite-suppressant drug used for the treatment of overweight and obesity. It has been suggested that the systemic and central activity of amfepramone produces cardiovascular effects such as transient ischemic attacks and primary pulmonary hypertension. However, it is not known whether amfepramone produces immediate vascular effects when applied in vitro to rat aortic rings and, if so, what mechanisms may be involved. We analyzed the effect of amfepramone on phenylephrine-precontracted rat aortic rings with or without endothelium and the influence of inhibitors or blockers on this effect. Amfepramone produced a concentration-dependent vasorelaxation in phenylephrine-precontracted rat aortic rings that was not affected by the vehicle, atropine, 4-AP, glibenclamide, indomethacin, clotrimazole, or cycloheximide. The vasorelaxant effect of amfepramone was significantly attenuated by NG-nitro-L-arginine methyl ester (L-NAME) and tetraethylammonium (TEA), and was blocked by removal of the vascular endothelium. These results suggest that amfepramone had a direct vasorelaxant effect on phenylephrine-precontracted rat aortic rings, and that inhibition of endothelial nitric oxide synthase and the opening of Ca2+-activated K+ channels were involved in this effect.
Descritores: Acetilcolina/farmacologia
Aorta Torácica/efeitos dos fármacos
Depressores do Apetite/farmacologia
Dietilpropiona/farmacologia
Vasodilatadores/farmacologia
-Aorta Torácica/metabolismo
Canais de Cálcio/efeitos dos fármacos
Canais de Cálcio/metabolismo
Endotélio Vascular/efeitos dos fármacos
NG-Nitroarginina Metil Éster/metabolismo
Óxido Nítrico Sintase Tipo III/efeitos dos fármacos
Fenilefrina/farmacologia
Canais de Potássio/efeitos dos fármacos
Canais de Potássio/metabolismo
Ratos Wistar
Tetraetilamônio/metabolismo
Vasoconstritores/farmacologia
Vasodilatação/efeitos dos fármacos
Limites: Animais
Masculino
Tipo de Publ: Estudo de Avaliação
Responsável: BR1.1 - BIREME


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Id: lil-731151
Autor: Higuita, Lina Maria Serna; Nieto-Ríos, John Fredy; Daguer-Gonzalez, Salomon; Ocampo-Kohn, Catalina; Aristizabal-Alzate, Arbey; Velez-Echeverri, Catalina; Vanegas-Ruiz, Juan Jose; Ramirez-Sanchez, Isabel; Tobon, Jhon Jairo Zuleta; Zuluaga-Valencia, Gustavo Adolfo.
Título: Tuberculosis in renal transplant patients: The experience of a single center in Medellín-Colombia, 2005-2013 / Tuberculose em pacientes transplantados renais: experiência de um único centro em Medellín-Colômbia, 2005-2013
Fonte: J. bras. nefrol;36(4):512-518, Oct-Dec/2014. tab.
Idioma: en.
Resumo: Introduction: Tuberculosis is a common opportunistic infection in renal transplant patients. Objective: To obtain a clinical and laboratory description of transplant patients diagnosed with tuberculosis and their response to treatment during a period ranging from 2005 to 2013 at the Pablo Tobón Uribe Hospital. Methods: Retrospective and descriptive study. Results: In 641 renal transplants, tuberculosis was confirmed in 12 cases. Of these, 25% had a history of acute rejection, and 50% had creatinine levels greater than 1.5 mg/dl prior to infection. The disease typically presented as pulmonary (50%) and disseminated (33.3%). The first phase of treatment consisted of 3 months of HZRE (isoniazid, pyrazinamide, rifampicin and ethambutol) in 75% of the cases and HZME (isoniazid, pyrazinamide, moxifloxacin and ethambutol) in 25% of the cases. During the second phase of the treatment, 75% of the cases received isoniazid and rifampicin, and 25% of the cases received isoniazid and ethambutol. The length of treatment varied between 6 and 18 months. In 41.7% of patients, hepatotoxicity was associated with the beginning of anti-tuberculosis therapy. During a year-long follow-up, renal function remained stable, and the mortality rate was 16.7%. Conclusion: Tuberculosis in the renal transplant population studied caused diverse nonspecific symptoms. Pulmonary and disseminated tuberculosis were the most frequent forms and required prolonged treatment. Antituberculosis medications had a high toxicity and mortality. This infection must be considered when patients present with a febrile syndrome of unknown origin, especially during the first year after renal transplant. .

Introdução: A tuberculose é uma infecção oportunista comum em pacientes transplantados renais. Objetivo: Oferecer uma descrição clínica e laboratorial de pacientes transplantados com diagnóstico de tuberculose e sua resposta ao tratamento durante o período entre 2005 e 2013 no Hospital Pablo Tobón Uribe. Métodos: Estudo retrospectivo descritivo. Resultados: Em 641 transplantes renais, a tuberculose foi confirmada em 12 pacientes. Destes, 25% tinham histórico de rejeição aguda e 50% apresentaram níveis de creatinina superiores a 1,5 mg/dl antes da infecção. A patologia geralmente se apresentava como pulmonar (50%) e disseminada (33,3%). A primeira fase do tratamento consistiu de três meses de HZRE (isoniazida, pirazinamida, rifampicina e etambutol) em 75% dos casos e HZME (isoniazida, pirazinamida, moxifloxacina e etambutol) em 25% dos pacientes. Durante a segunda fase do tratamento, 75% dos pacientes receberam isoniazida e rifampicina e 25% isoniazida e etambutol. A duração do tratamento variou entre seis e 18 meses. Em 41,7% dos pacientes, hepatotoxicidade foi associada ao início do tratamento da tuberculose. Durante o seguimento de um ano a função renal manteve-se estável e a taxa de mortalidade foi de 16,7%. Conclusão: A tuberculose foi responsável por diversos sintomas inespecíficos na população de transplantados renais estudada. Tuberculose pulmonar e disseminada foram as formas mais frequentes de acometimento e necessitaram de tratamento prolongado. Medicamentos contra a tuberculose apresentaram alta toxicidade e mortalidade. Esta infecção deve ser considerada quando o paciente apresenta síndrome febril de origem desconhecida, especialmente durante o primeiro ano após o transplante renal. .
Descritores: Locus Cerúleo/efeitos dos fármacos
Entorpecentes/farmacologia
Inibição Neural/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Canais de Potássio/metabolismo
-Bário/farmacologia
Cálcio/metabolismo
Encefalina Metionina/farmacologia
Canais de Potássio Corretores do Fluxo de Internalização Acoplados a Proteínas G
Proteínas de Ligação ao GTP/metabolismo
Heterozigoto
Homozigoto
Ativação do Canal Iônico/efeitos dos fármacos
Ativação do Canal Iônico/fisiologia
Locus Cerúleo/citologia
Locus Cerúleo/fisiologia
Camundongos Knockout
Potenciais da Membrana/efeitos dos fármacos
Potenciais da Membrana/fisiologia
Inibição Neural/fisiologia
Neurônios/fisiologia
Técnicas de Patch-Clamp
Subunidades Proteicas
Bloqueadores dos Canais de Potássio/farmacologia
Canais de Potássio Corretores do Fluxo de Internalização/antagonistas & inibidores
Canais de Potássio Corretores do Fluxo de Internalização/deficiência
Canais de Potássio Corretores do Fluxo de Internalização/genética
Canais de Potássio Corretores do Fluxo de Internalização/metabolismo
Canais de Potássio/deficiência
Canais de Potássio/genética
Limites: Animais
Feminino
Masculino
Camundongos
Tipo de Publ: Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Responsável: BR1.1 - BIREME


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Id: lil-672661
Autor: Khanna, N; Malhotra, RS; Mehta, AK; Garg, GR; Halder, S; Sharma, KK.
Título: Potassium channel openers exhibit cross-tolerance with morphine in two experimental models of pain / Los abridores de canales de potasio exhiben tolerancia cruzada con la morfina en dos modelos experimentales de dolor
Fonte: West Indian med. j;59(5):473-478, Oct. 2010. tab.
Idioma: en.
Resumo: OBJECTIVE: The study was performed to assess the effect of potassium channel openers on morphine tolerance and vice-versa. METHODS: Swiss albino mice of either gender weighing between 25-30 g were used for the study. The study assesses the effect of potassium channel openers (cromakalim, diazoxide and minoxidil) on morphine tolerance and vice-versa, using formalin and tail-flick tests. RESULTS: The antinociceptive effect of cromakalim and minoxidil was significantly reduced when administered to morphine-tolerant mice, in both the behavioural tests. However, reduced analgesic effect of diazoxide was observed on morphine-tolerance in the formalin test but not in the tail-flick test. Tolerance was observed when morphine was administered to animals chronically treated with any of the potassium channel openers. The same effect was observed when morphine was injected into a group treated with a combination of morphine and any of the potassium channel openers. CONCLUSIONS: This study, therefore, suggests that both morphine and potassium channel openers are cross-tolerant. However, such interaction occurs at the level of potassium channels rather than at the level of receptors.

OBJETIVO: El estudio fue realizado para evaluar el efecto de los abridores de canales de potasio en la tolerancia a la morfina, y viceversa. MÉTODOS: Para el estudio, se usaron ratones albinos suizos de ambos sexos que pesaban entre 25-30 g. El estudio evalúa el efecto de los abridores de canales de potasio (cromacalina, diazóxido y minoxidil) en la tolerancia a la morfina, y viceversa, usando la prueba de la sacudida de la cola y la prueba de la formalina. RESULTADOS: El efecto antinociceptivo de la cromacalina y el minoxidil fue significativamente reducido cuando se le administró a los ratones tolerantes a la morfina, en ambas pruebas conductuales. Sin embargo, se observó un efecto analgésico reducido de diazóxido sobre la tolerancia a la morfina en la prueba de la formalina, pero no en la prueba de la sacudida de la cola. Se observó tolerancia al administrar morfina a animales crónicamente tratados con cualquiera de los abridores de canales de potasio. El mismo efecto fue observado cuando se inyectó la morfina al grupo tratado con una combinación de morfina y cualquiera de los abridores de canales de potasio. CONCLUSIONES: Por consiguiente, este estudio sugiere que tanto la morfina como los abridores de canales de potasio son tolerantes cruzados. Sin embargo, tal interacción ocurre a nivel de los canales de potasio más bien que a nivel de los receptores.
Descritores: Analgésicos Opioides/farmacologia
Cromakalim/farmacologia
Tolerância a Medicamentos
Diazóxido/farmacologia
Minoxidil/farmacologia
Morfina/farmacologia
Canais de Potássio/efeitos dos fármacos
-Ativação do Canal Iônico/efeitos dos fármacos
Modelos Animais
Dor
Limites: Animais
Camundongos
Responsável: BR1.1 - BIREME


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Moraes, Maria Elisabete Amaral de
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Id: lil-655997
Autor: Cerqueira, João Batista Gadelha de; Gonzaga-Silva, Lúcio Flávio; Silva, Francisco Ordelei Nascimento da; Cerqueira, João Victor Medeiros de; Oliveira, Ricardo Reges Maia; Moraes, Maria Elisabete Amaral de; Nascimento, Nilberto Robson Falcão do.
Título: Identification of mechanisms involved in the relaxation of rabbit cavernous smooth muscle by a new nitric oxide donor ruthenium compound
Fonte: Int. braz. j. urol;38(5):687-694, Sept.-Oct. 2012. ilus.
Idioma: en.
Resumo: PURPOSE: The aim of this study was to evaluate the relaxation in vitro of cavernous smooth muscle induced by a new NO donor of the complex nitrosil-ruthenium, named trans-[Ru(NH3)4(caffeine)(NO)]C13 (Rut-Caf) and sodium nitroprusside (SNP). MATERIALS AND METHODS: The tissues, immersed in isolated bath systems, were pre-contracted with phenilephrine (PE) (1 µM) and then concentration-response curves (10-12 - 10-4 M) were obtained. To clarify the mechanism of action involved, it was added to the baths ODQ (10 µM, 30 µM), oxyhemoglobin (10 µM), L-cysteine (100 µM), hydroxicobalamine (100 µM), glibenclamide, iberotoxin and apamine. Tissue samples were frozen in liquid nitrogen to measure the amount of cGMP and cAMP produced. RESULTS: The substances provoked significant relaxation of the cavernous smooth muscle. Both Rut-Caf and SNP determined dose-dependent relaxation with similar potency (pEC50) and maximum effect (Emax). The substances showed activity through activation of the soluble guanylyl cyclase (sGC), because the relaxations were inhibited by ODQ. Oxyhemoglobin significantly diminished the relaxation effect of the substances. L-cysteine failed to modify the relaxations caused by the agents. Hydroxicobalamine significantly diminished the relaxation effect of Rut-Caf. Glibenclamide significantly increased the efficacy of Rut-Caf (pEC50 4.09 x 7.09). There were no alterations of potency or maximum effect of the substances with the addition of the other ion channel blockers. Rut-Caf induced production of significant amounts of cGMP and cAMP during the relaxation process. CONCLUSIONS: In conclusion, Rut-Caf causes relaxation of smooth muscle of corpus cavernosum by means of activation of sGC with intracellular production of cGMP and cAMP; and also by release of NO in the intracellular environment. Rut-Caf releases the NO free radical and it does not act directly on the potassium ion channels.
Descritores: Relaxamento Muscular/fisiologia
Músculo Liso/efeitos dos fármacos
Doadores de Óxido Nítrico/farmacologia
Nitroprussiato/farmacologia
Compostos de Rutênio/farmacologia
-GMP Cíclico/biossíntese
GMP Cíclico/química
Cisteína/farmacologia
Guanosina Monofosfato/biossíntese
Guanosina Monofosfato/química
Músculo Liso/fisiologia
Doadores de Óxido Nítrico/química
Nitroprussiato/química
Canais de Potássio/química
Compostos de Rutênio/química
Fatores de Tempo
Limites: Animais
Masculino
Coelhos
Responsável: BR1.1 - BIREME


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Id: lil-632392
Autor: Medeiros-Domingo, Argelia; Iturralde-Torres, Pedro; Cañizales-Quinteros, Samuel; Hernández-Cruz, Arturo; Tusié-Luna, Ma. Teresa.
Título: Nuevas perspectivas en el síndrome de QT largo / New perspectives in long QT syndrome
Fonte: Rev. invest. clín;59(1):57-72, ene.-feb. 2007. ilus, tab.
Idioma: es.
Resumo: Long QT Syndrome (LQTS) is a cardiac channelopathy characterized by prolonged ventricular repolarization and increased risk to sudden death secondary to ventricular dysrrhythmias. Was the first cardiac channelopathy described and is probably the best understood. After a decade of the sentinel identification of ion channel mutation in LQTS, genotype-phenotype correlations have been developed along with important improvement in risk stratification and genetic guided-treatment. Genetic screening has shown that LQTS is more frequent than expected and interestingly, ethnic specific polymorphism conferring increased susceptibility to drug induced QT prolongation and torsades de pointes have been identified. A better understanding of ventricular arrhythmias as an adverse effect of ion channel binding drugs, allow the development of more safety formulas and better control of this public health problem. Progress in understanding the molecular basis of LQTS has been remarkable; eight different genes have been identified, however still 25% of patients remain genotype-negative. This article is an overview of the main LQTS knowledge developed during the last years.

El síndrome de QT largo (SQTL) es una canalopatía que genera grave alteración en la repolarización ventricular predispone a arritmias malignas y muerte súbita. Fue la primera canalopatía arritmogénica descrita y quizá la mejor entendida hasta ahora. Transcurrida ya más de una década de la identificación de la primera mutación asociada al SQTL, se ha hecho evidente que este trastorno es mucho más frecuente de lo que inicialmente se pensaba; los avances en el conocimiento de la fisiopatología molecular de esta enfermedad han permitido hacer una correlación genotipo-fenotipo, optimizando el tratamiento y permitiendo estratificar el riesgo en forma precisa. Se ha logrado entender con mayor detalle los efectos adversos de distintas drogas que interactúan con los canales iónicos, permitiendo así generar fármacos más seguros y, en su defecto, monitorizar de cerca aquellos que a pesar de tener este efecto adverso, es necesaria su administración. Los avances son importantes pero no todo está dicho, 25% de los casos no tienen mutaciones en los genes descritos hasta la fecha, por lo que el SQTL continúa siendo motivo de investigación. El presente artículo constituye un resumen de los principales conceptos desarrollados en los últimos diez años que han sido cruciales en el manejo de esta enfermedad.
Descritores: Síndrome do QT Longo
-Bradicardia/diagnóstico
Bradicardia/embriologia
Bradicardia/genética
Fármacos Cardiovasculares/uso terapêutico
Morte Súbita Cardíaca/etiologia
Cardioversão Elétrica
Doenças Fetais/diagnóstico
Doenças Fetais/genética
Coração Fetal/fisiopatologia
Ganglionectomia
Genótipo
Transporte de Íons/genética
Síndrome do QT Longo/induzido quimicamente
Síndrome do QT Longo/classificação
Síndrome do QT Longo/complicações
Síndrome do QT Longo/diagnóstico
Síndrome do QT Longo/embriologia
Síndrome do QT Longo/epidemiologia
Síndrome do QT Longo/genética
Síndrome do QT Longo/terapia
Marca-Passo Artificial
Fenótipo
Diagnóstico Pré-Natal
Canais de Potássio/genética
Canais de Potássio/fisiologia
Canais de Sódio/genética
Canais de Sódio/fisiologia
Gânglio Estrelado/cirurgia
Taquicardia Ventricular/etiologia
Torsades de Pointes/etiologia
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Revisão
Responsável: MX1.1 - CENIDSP - Centro de Información para Decisiones en Salud Pública



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