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[PMID]:28831600
[Au] Autor:Candelaria M; Burgos S; Ponce M; Espinoza R; Dueñas-Gonzalez A
[Ad] Endereço:Division de Investigación Clínica, Instituto Nacional de Cancerología, Av. San Fernando 22, Tlalpan, 14080, México, D.F., Mexico. candelariahmgloria@gmail.com.
[Ti] Título:Encouraging results with the compassionate use of hydralazine/valproate (TRANSKRIP™) as epigenetic treatment for myelodysplastic syndrome (MDS).
[So] Source:Ann Hematol;96(11):1825-1832, 2017 Nov.
[Is] ISSN:1432-0584
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The hypomethylating agents azacytidine and decitabine are unaffordable for many patients with MDS. The combination of the DNA methyltransferase inhibitor hydralazine and the histone deacetylase inhibitor valproate has shown preliminary efficacy in MDS. The aim of this study is to evaluate the clinical efficacy and safety of hydralazine/valproate in a case series of MDS patients treated in a compassionate manner. Hydralazine was dosed according to the acetylation genotype of patients (slow acetylators 83 mg daily; fast acetylators 182 mg daily), and valproate was dosed at 30 mg/kg/day. Both drugs were given daily until disease progression. Response and toxicity were evaluated with the International Working Group criteria and CTCAE, version 4, respectively. Survival parameters were estimated with the Kaplan-Meier method. From 2009 to 2012, 14 patients were treated. The median age ± SD was 55.2 ± 19.52 (range 23-87) years. According to the IPSS, cases were graded as intermediate-1 (n = 8/14; 57.2%) or intermediate-2 (n = 6/14; 42.8%). Responses were as follows: five (35.7%) complete response, one (7.1%) partial response, and two (14.28%) became transfusion independent. The mean duration of response ± SD was 60 ± 35.28 months (range 5-94). Three patients progressed to AML. At a median follow-up of 57 months (range 1-106), the median OS was 27 months. At that point, five patients remained on the treatment, one with partial response and four with complete response. The median OS was not reached in the eight patients who saw a clinical benefit from the treatment, in comparison to an OS of 7 months in the six patients who had no treatment. The combination of hydralazine and valproate is safe and effective in MDS, and its further testing is highly desirable.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Ensaios de Uso Compassivo/métodos
Epigênese Genética/efeitos dos fármacos
Hidralazina/administração & dosagem
Síndromes Mielodisplásicas/tratamento farmacológico
Ácido Valproico/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Ensaios de Uso Compassivo/mortalidade
Epigênese Genética/fisiologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Síndromes Mielodisplásicas/diagnóstico
Síndromes Mielodisplásicas/mortalidade
Estudos Retrospectivos
Taxa de Sobrevida/tendências
Resultado do Tratamento
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
26NAK24LS8 (Hydralazine); 614OI1Z5WI (Valproic Acid)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170824
[St] Status:MEDLINE
[do] DOI:10.1007/s00277-017-3103-x


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[PMID]:28738383
[Au] Autor:Chatard M; Puech C; Perek N; Roche F
[Ad] Endereço:Univ Lyon, UJM-Saint-Etienne, SNA-EPIS, EA4607, Saint-Etienne, France.
[Ti] Título:Hydralazine is a Suitable Mimetic Agent of Hypoxia to Study the Impact of Hypoxic Stress on In Vitro Blood-Brain Barrier Model.
[So] Source:Cell Physiol Biochem;42(4):1592-1602, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Understanding cellular mechanisms induced by hypoxia is fundamental to reduce blood-brain barrier (BBB) disruption. Nevertheless, the investigation of hypoxia on cellular pathways is complex with true hypoxia because HIF-1α has a short lifetime and rapidly reverts back to a normoxic state. To overcome this difficulty, mimetic agents of the hypoxia pathway have been developed, including the gold standard CoCl2. In this study, we proposed to compare CoCl2 and hydralazine in order to determine a suitable mimetic agent of hypoxia for the study on the BBB. METHODS: We studied the cytotoxicity and the impact of these molecules on the integrity of an in vitro BBB model by comparing them to hypoxia controls. RESULTS: We showed that the impact of hypoxic stress in our in vitro BBB model is rather similar between hydralazine and CoCl2. Chemical hypoxic stress led to an increase of BBB permeability either with CoCl2 or hydralazine. Tight junction protein expressions showed that this chemical hypoxic stress decreased ZO-1 but not occluding expressions, and cells had set up a defence mechanism by increasing expression and activity of their efflux transporters. CONCLUSION: Our results demonstrated that hydralazine is a better mimetic agent and more suitable than CoCl2 because it had the same effect but without the cytotoxic effect on in vitro BBB cells.
[Mh] Termos MeSH primário: Barreira Hematoencefálica/efeitos dos fármacos
Células Endoteliais/efeitos dos fármacos
Hidralazina/farmacologia
Neuroglia/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Transporte Biológico/efeitos dos fármacos
Barreira Hematoencefálica/metabolismo
Hipóxia Celular/efeitos dos fármacos
Linhagem Celular Transformada
Linhagem Celular Tumoral
Sobrevivência Celular/efeitos dos fármacos
Cobalto/farmacologia
Técnicas de Cocultura
Células Endoteliais/citologia
Células Endoteliais/metabolismo
Fluoresceína/metabolismo
Fluoresceínas/metabolismo
Corantes Fluorescentes/metabolismo
Regulação da Expressão Gênica
Subunidade alfa do Fator 1 Induzível por Hipóxia/genética
Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo
Camundongos
Modelos Biológicos
Neuroglia/citologia
Neuroglia/metabolismo
Ocludina/genética
Ocludina/metabolismo
Permeabilidade/efeitos dos fármacos
Ratos
Proteína da Zônula de Oclusão-1/genética
Proteína da Zônula de Oclusão-1/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fluoresceins); 0 (Fluorescent Dyes); 0 (Hif1a protein, mouse); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); 0 (Occludin); 0 (Ocln protein, mouse); 0 (Tjp1 protein, mouse); 0 (Zonula Occludens-1 Protein); 26NAK24LS8 (Hydralazine); 3G0H8C9362 (Cobalt); 85138-49-4 (2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein); EVS87XF13W (cobaltous chloride); TPY09G7XIR (Fluorescein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170725
[St] Status:MEDLINE
[do] DOI:10.1159/000479399


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[PMID]:28295336
[Au] Autor:Parker LM; Le S; Wearne TA; Hardwick K; Kumar NN; Robinson KJ; McMullan S; Goodchild AK
[Ad] Endereço:Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University, NSW, 2109, Australia.
[Ti] Título:Neurochemistry of neurons in the ventrolateral medulla activated by hypotension: Are the same neurons activated by glucoprivation?
[So] Source:J Comp Neurol;525(9):2249-2264, 2017 Jun 15.
[Is] ISSN:1096-9861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Previous studies have demonstrated that a range of stimuli activate neurons, including catecholaminergic neurons, in the ventrolateral medulla. Not all catecholaminergic neurons are activated and other neurochemical content is largely unknown hence whether stimulus specific populations exist is unclear. Here we determine the neurochemistry (using in situ hybridization) of catecholaminergic and noncatecholaminergic neurons which express c-Fos immunoreactivity throughout the rostrocaudal extent of the ventrolateral medulla, in Sprague Dawley rats treated with hydralazine or saline. Distinct neuronal populations containing PPCART, PPPACAP, and PPNPY mRNAs, which were largely catecholaminergic, were activated by hydralazine but not saline. Both catecholaminergic and noncatecholaminergic neurons containing preprotachykinin and prepro-enkephalin (PPE) mRNAs were also activated, with the noncatecholaminergic population located in the rostral C1 region. Few GlyT2 neurons were activated. A subset of these data was then used to compare the neuronal populations activated by 2-deoxyglucose evoked glucoprivation (Brain Structure and Function (2015) 220:117). Hydralazine activated more neurons than 2-deoxyglucose but similar numbers of catecholaminergic neurons. Commonly activated populations expressing PPNPY and PPE mRNAs were defined. These likely include PPNPY expressing catecholaminergic neurons projecting to vasopressinergic and corticotrophin releasing factor neurons in the paraventricular nucleus, which when activated result in elevated plasma vasopressin and corticosterone. Stimulus specific neurons included noncatecholaminergic neurons and a few PPE positive catecholaminergic neuron but neurochemical codes were largely unidentified. Reasons for the lack of identification of stimulus specific neurons, readily detectable using electrophysiology in anaesthetized preparations and for which neural circuits can be defined, are discussed.
[Mh] Termos MeSH primário: Bulbo/citologia
Neuroquímica
Neurônios/efeitos dos fármacos
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Animais
Anti-Hipertensivos/farmacologia
Catecolaminas/metabolismo
Desoxiglucose/farmacologia
Encefalinas/genética
Encefalinas/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Proteínas da Membrana Plasmática de Transporte de Glicina/genética
Proteínas da Membrana Plasmática de Transporte de Glicina/metabolismo
Hidralazina/farmacologia
Hipotensão/metabolismo
Hipotensão/patologia
Masculino
Proteínas do Tecido Nervoso/genética
Proteínas do Tecido Nervoso/metabolismo
Neuropeptídeo Y/genética
Neuropeptídeo Y/metabolismo
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/genética
Polipeptídeo Hipofisário Ativador de Adenilato Ciclase/metabolismo
Precursores de Proteínas/genética
Precursores de Proteínas/metabolismo
Proteínas Proto-Oncogênicas c-fos/genética
Proteínas Proto-Oncogênicas c-fos/metabolismo
Ratos
Ratos Sprague-Dawley
Taquicininas/genética
Taquicininas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adcyap1 protein, rat); 0 (Antihypertensive Agents); 0 (Catecholamines); 0 (Enkephalins); 0 (Glycine Plasma Membrane Transport Proteins); 0 (Nerve Tissue Proteins); 0 (Neuropeptide Y); 0 (Pituitary Adenylate Cyclase-Activating Polypeptide); 0 (Protein Precursors); 0 (Proto-Oncogene Proteins c-fos); 0 (Slc6a5 protein, rat); 0 (Tachykinins); 0 (cocaine- and amphetamine-regulated transcript protein); 0 (preprotachykinin); 26NAK24LS8 (Hydralazine); 93443-35-7 (preproenkephalin); 9G2MP84A8W (Deoxyglucose)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170825
[Lr] Data última revisão:
170825
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170316
[St] Status:MEDLINE
[do] DOI:10.1002/cne.24203


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[PMID]:28277033
[Au] Autor:Espinoza-Zamora JR; Labardini-Méndez J; Sosa-Espinoza A; López-González C; Vieyra-García M; Candelaria M; Lozano-Zavaleta V; Toledano-Cuevas DV; Zapata-Canto N; Cervera E; Dueñas-González A
[Ad] Endereço:a Department of Hematology , Instituto Nacional de Cancerología , Mexico City , Mexico.
[Ti] Título:Efficacy of hydralazine and valproate in cutaneous T-cell lymphoma, a phase II study.
[So] Source:Expert Opin Investig Drugs;26(4):481-487, 2017 Apr.
[Is] ISSN:1744-7658
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To evaluate the activity and safety of hydralazine and valproate (Transkrip) in cutaneous T-cell lymphoma (CTCL). METHODS: Previously untreated and progressive/refractory CTCL patients received hydralazine at 83 mg or 182 mg/day for slow and rapid acetylators respectively plus magnesium valproate at a total dose of 30 mg/Kg t.i.d daily in continuous 28-day cycles in this phase II study. The primary objective was overall response rate (ORR) measured by the modified severity weighted assessment tool (m-SWAT), secondary end-points were time to response (TTR), time to progression (TTP), duration of response (DOR), progression-free survival (PFS), overall survival (OS) and safety. RESULTS: Fourteen patients were enrolled (7 untreated and 7 pretreated). ORR was 71% with 50% complete and 21% partial. Two had stable disease and two progressed. At a median follow-up of 36 months (5-52), median TTR was 2 months (1-4); median DOR was 28 months (5-45); median PFS 36 and not reached for OS. There were no differences in median TTR, DOR, and PFS between treated and pretreated patients. Pruritus relieve was complete in 13 out of 14 patients. No grade 3 or 4 toxicities were observed. CONCLUSION: The combination of hydralazine and valproate is safe, very well tolerated and effective in CTCL.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Linfoma Cutâneo de Células T/tratamento farmacológico
Prurido/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Protocolos de Quimioterapia Combinada Antineoplásica/efeitos adversos
Intervalo Livre de Doença
Feminino
Seguimentos
Seres Humanos
Hidralazina/administração & dosagem
Linfoma Cutâneo de Células T/patologia
Masculino
Meia-Idade
Prurido/etiologia
Taxa de Sobrevida
Fatores de Tempo
Resultado do Tratamento
Ácido Valproico/administração & dosagem
Adulto Jovem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE
[Nm] Nome de substância:
26NAK24LS8 (Hydralazine); 614OI1Z5WI (Valproic Acid)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170404
[Lr] Data última revisão:
170404
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1080/13543784.2017.1291630


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[PMID]:28189913
[Au] Autor:Linnekamp JF; Butter R; Spijker R; Medema JP; van Laarhoven HW
[Ad] Endereço:Laboratory of Experimental Oncology and Radiobiology (LEXOR), Center for Experimental Molecular Medicine (CEMM), Academic Medical Center (AMC), University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands; Cancer Center Amsterdam and Cancer Genomics Center, Amsterdam, The Netherlands.
[Ti] Título:Clinical and biological effects of demethylating agents on solid tumours - A systematic review.
[So] Source:Cancer Treat Rev;54:10-23, 2017 Mar.
[Is] ISSN:1532-1967
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: It is assumed that DNA methylation plays a key role in both tumour development and therapy resistance. Demethylating agents have been shown to be effective in the treatment of haematological malignancies. Based on encouraging preclinical results, demethylating agents may also be effective in solid tumours. This systematic review summarizes the evidence of the effect of demethylating agents on clinical response, methylation and the immune system in solid tumours. METHODS: We conducted a systematic literature search from 1949 to December 2016, according to the PRISMA guidelines. Studies which evaluated treatment with azacitidine, decitabine, guadecitabine, hydralazine, procaine, MG98 and/or zebularine in patients with solid tumours were included. Data on clinical response, effects on methylation and immune response were extracted. RESULTS: Fifty-eight studies were included: in 13 studies complete responses (CR) were observed, 35 studies showed partial responses (PR), 47 studies stable disease (SD) and all studies except two showed progressive disease (PD). Effects on global methylation were observed in 11/15 studies and demethylation/re-expression of tumour specific genes was seen in 15/17 studies. No clear correlation between (de)methylation and clinical response was observed. In 14 studies immune-related responses were reported, such as re-expression of cancer-testis antigens and upregulation of interferon genes. CONCLUSION: Demethylating agents are able to improve clinical outcome and alter methylation status in patients with solid tumours. Although beneficial effect has been shown in individual patients, overall response is limited. Further research on biomarker predicting therapy efficacy is indicated, particularly in earlier stage and highly methylated tumours.
[Mh] Termos MeSH primário: Antimetabólitos Antineoplásicos/uso terapêutico
Neoplasias/tratamento farmacológico
[Mh] Termos MeSH secundário: Azacitidina/análogos & derivados
Azacitidina/uso terapêutico
Citidina/análogos & derivados
Citidina/uso terapêutico
Metilação de DNA/efeitos dos fármacos
Seres Humanos
Hidralazina/uso terapêutico
Sistema Imunitário/efeitos dos fármacos
Metilação/efeitos dos fármacos
Neoplasias/imunologia
Neoplasias/metabolismo
Neoplasias/radioterapia
Procaína/uso terapêutico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Antimetabolites, Antineoplastic); 26NAK24LS8 (Hydralazine); 2KT4YN1DP7 (guadecitabine); 4Z8Y51M438 (Procaine); 5CSZ8459RP (Cytidine); 776B62CQ27 (decitabine); 7A9Y5SX0GY (pyrimidin-2-one beta-ribofuranoside); M801H13NRU (Azacitidine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170213
[St] Status:MEDLINE


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[PMID]:28069864
[Au] Autor:Kawasaki S; Kako K; Nagashima Y; Kanou A; Ishida J; Fukamizu A
[Ad] Endereço:Graduate School of Life and Environmental Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8577, Japan.
[Ti] Título:Hydralazine is involved in tele-methylhistamine metabolism by inhibiting monoamine oxidase B in pregnancy-associated hypertensive mice.
[So] Source:J Biochem;161(2):155-158, 2017 Feb 01.
[Is] ISSN:1756-2651
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hypertensive disorders of pregnancy globally affect 6-8% of gestation and remain a major cause of both foetal and maternal morbidity and mortality. However, the antihypertensive medications for the patients of this disease are strictly limited due to the teratogenic potentials. Here, we found that tele-methylhistamine (tMH) increased in response to the administration of hydralazine (Hdz), a vasodilative agent, in the pregnancy-associated hypertensive (PAH) mice. Hdz abrogated the degradation of tMH catalyzed by monoamine oxidase B (MAO-B) in vitro. These results suggested that Hdz inhibited the MAO-B activity and consequently tMH increased in the maternal circulation of PAH mice.
[Mh] Termos MeSH primário: Hidralazina/farmacologia
Hipertensão Induzida pela Gravidez/tratamento farmacológico
Metilistaminas/metabolismo
Monoaminoxidase/metabolismo
[Mh] Termos MeSH secundário: Aminas/sangue
Animais
Anti-Hipertensivos/farmacologia
Biocatálise/efeitos dos fármacos
Cromatografia Líquida de Alta Pressão/métodos
Feminino
Seres Humanos
Hipertensão Induzida pela Gravidez/enzimologia
Hipertensão Induzida pela Gravidez/metabolismo
Metilistaminas/sangue
Camundongos
Gravidez
Espectrometria de Massas por Ionização e Dessorção a Laser Assistida por Matriz
Especificidade por Substrato
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amines); 0 (Antihypertensive Agents); 0 (Methylhistamines); 26NAK24LS8 (Hydralazine); EC 1.4.3.4 (Monoamine Oxidase); KCB81T4EOF (tele-methylhistamine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170111
[St] Status:MEDLINE
[do] DOI:10.1093/jb/mvw090


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[PMID]:27998008
[Au] Autor:Xu B; Bobek G; Makris A; Hennessy A
[Ad] Endereço:School of Medicine, Western Sydney University, Sydney, NSW, Australia.
[Ti] Título:Antihypertensive methyldopa, labetalol, hydralazine, and clonidine reversed tumour necrosis factor-α inhibited endothelial nitric oxide synthase expression in endothelial-trophoblast cellular networks.
[So] Source:Clin Exp Pharmacol Physiol;44(3):421-427, 2017 Mar.
[Is] ISSN:1440-1681
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Medications used to control hypertension in pregnancy also improve trophoblast and endothelial cellular interaction in vitro. Tumour necrosis factor-α (TNF-α) inhibits trophoblast and endothelial cellular interactions and simultaneously decreases endothelial nitric oxide synthase (eNOS) expression. This study investigated whether antihypertensive medications improved these cellular interactions by modulating eNOS and inducible nitric oxide synthase (iNOS) expression. Human uterine myometrial microvascular endothelial cells (UtMVECs) were pre-incubated with (or without) low dose TNF-α (0.5 ng/mL) or TNF-α plus soluble fms-like tyrosine kinase-1 (sFlt-1) (100 ng/mL). The endothelial cells were cultured on Matrigel. After endothelial cellular networks appeared, trophoblast derived HTR-8/SVneo cells were co-cultured in the presence of clinically relevant doses of methyldopa, labetalol, hydralazine or clonidine for 24 hours. Cells were retrieved from the Matrigel to extract mRNA and eNOS and iNOS expression were examined by quantitative PCR. Methyldopa, labetalol, hydralazine and clonidine reversed the inhibitory effect of TNF-α on eNOS mRNA expression. After pre-incubating endothelial cells with TNF-α and sFlt-1, all the medications except methyldopa lost their effect on eNOS mRNA expression. In the absence of TNF-α, antihypertensive medications did not change eNOS expression. The mRNA expression of iNOS was not affected by TNF-α or any medications. This study shows that selected antihypertensive medications used in the treatment of hypertension in pregnancy increase eNOS expression in vitro when induced by the inflammatory TNF-α. The anti-angiogenic molecule sFlt-1 may antagonise the potential benefit of these medications by interfering with the NOS pathway.
[Mh] Termos MeSH primário: Anti-Hipertensivos/farmacologia
Células Endoteliais/efeitos dos fármacos
Óxido Nítrico Sintase Tipo III/antagonistas & inibidores
Trofoblastos/efeitos dos fármacos
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Células Cultivadas
Clonidina/farmacologia
Técnicas de Cocultura
Meios de Cultivo Condicionados
Células Endoteliais/citologia
Endotélio Vascular/citologia
Endotélio Vascular/efeitos dos fármacos
Feminino
Seres Humanos
Hidralazina/farmacologia
Proteína 1 Semelhante a Receptor de Interleucina-1/fisiologia
Labetalol/farmacologia
Metildopa/farmacologia
Óxido Nítrico Sintase Tipo III/genética
Trofoblastos/citologia
Útero/citologia
Útero/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Culture Media, Conditioned); 0 (IL1RL1 protein, human); 0 (Interleukin-1 Receptor-Like 1 Protein); 0 (Tumor Necrosis Factor-alpha); 26NAK24LS8 (Hydralazine); 56LH93261Y (Methyldopa); EC 1.14.13.39 (NOS3 protein, human); EC 1.14.13.39 (Nitric Oxide Synthase Type III); MN3L5RMN02 (Clonidine); R5H8897N95 (Labetalol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161221
[St] Status:MEDLINE
[do] DOI:10.1111/1440-1681.12712


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Mill, José Geraldo
Texto completo
[PMID]:27915452
[Au] Autor:Rodrigues Junior LF; de Azevedo Carvalho AC; Pimentel EB; Mill JG; Nascimento JH
[Ad] Endereço:Institute of Biophysics Carlos Chagas Filho, Laboratory of Cardiac Electrophysiology Antonio Paes de Carvalho, Federal University of Rio de Janeiro, Av. Carlos Chagas Filho, 373 - CCS Bloco G - Ilha do Fundao, 21, Rio de Janeiro, RJ, 941-902, Brazil.
[Ti] Título:Chronic enalapril treatment increases transient outward potassium current in cardiomyocytes isolated from right ventricle of spontaneously hypertensive rats.
[So] Source:Naunyn Schmiedebergs Arch Pharmacol;390(3):225-234, 2017 Mar.
[Is] ISSN:1432-1912
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:It has been well established that chronic pressure overload resulting from hypertension leads to ventricular hypertrophy and electrophysiological remodeling. The transient outward potassium current (I ) reduction described in hypertensive animals delays ventricular repolarization, leading to complex ventricular arrhythmias and sudden death. Antihypertensive drugs, as angiotensin-converting enzyme inhibitors (ACEi), can restore I and reduce the incidence of arrhythmic events. The purpose of this study was to evaluate the differential effects of long-term treatment with ACEi or direct-acting smooth muscle relaxant on the I of left and right ventricle myocytes of spontaneously hypertensive rats (SHR). Animals were divided into four groups: normotensive Wistar-Kyoto rats (WKY), hypertensive (SHR), SHR treated for 6 weeks with enalapril 10 mg/kg/day (SHRE), or hydralazine 20 mg/kg/day (SHRH). Systolic blood pressure (SBP) and hypertrophy index (heart weight/body weight (HW/BW)) were determined at the end of treatment period. Cell membrane capacitance (C ) and I were assessed in cardiomyocytes isolated from left and right ventricles. The SHR exhibited significantly increased SBP and HW/BW when compared to the WKY. The treated groups, SHRE and SHRH, restored normal SBP but not HW/BW. The SHR group exhibited a diminished I in the left but not the right ventricle. Both the treated groups restored I in the left ventricle. However, in the right ventricle, only enalapril treatment modified I . The SHRE group exhibited a significant increase in I compared to all the other groups. These findings suggest that enalapril may increase I by a pressure overload independent mechanism.
[Mh] Termos MeSH primário: Inibidores da Enzima Conversora de Angiotensina/farmacologia
Anti-Hipertensivos/farmacologia
Enalapril/farmacologia
Ventrículos do Coração/efeitos dos fármacos
Hipertensão/tratamento farmacológico
Miócitos Cardíacos/efeitos dos fármacos
Canais de Potássio/efeitos dos fármacos
Potássio/metabolismo
[Mh] Termos MeSH secundário: Animais
Pressão Sanguínea/efeitos dos fármacos
Cardiomegalia/fisiopatologia
Modelos Animais de Doenças
Capacitância Elétrica
Ventrículos do Coração/metabolismo
Ventrículos do Coração/fisiopatologia
Hidralazina/farmacologia
Hipertensão/metabolismo
Hipertensão/fisiopatologia
Masculino
Potenciais da Membrana
Miócitos Cardíacos/metabolismo
Canais de Potássio/metabolismo
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Fatores de Tempo
Vasodilatadores/farmacologia
Função Ventricular Esquerda/efeitos dos fármacos
Função Ventricular Direita/efeitos dos fármacos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Antihypertensive Agents); 0 (Potassium Channels); 0 (Vasodilator Agents); 26NAK24LS8 (Hydralazine); 69PN84IO1A (Enalapril); RWP5GA015D (Potassium)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161205
[St] Status:MEDLINE
[do] DOI:10.1007/s00210-016-1322-7


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[PMID]:27748260
[Au] Autor:Magro CM; Momtahen S; Harp J
[Ad] Endereço:Department of Pathology and Laboratory Medicine.
[Ti] Título:The distinctive histopathology of hydralazine-associated ANCA positive vasculitis: in vivo demonstration of NETosis.
[So] Source:Eur J Dermatol;27(1):91-92, 2017 Feb 01.
[Is] ISSN:1952-4013
[Cp] País de publicação:France
[La] Idioma:eng
[Mh] Termos MeSH primário: Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/induzido quimicamente
Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/patologia
Anti-Hipertensivos/efeitos adversos
Erupção por Droga/patologia
Hidralazina/efeitos adversos
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Vasculite Associada a Anticorpo Anticitoplasma de Neutrófilos/metabolismo
Erupção por Droga/etiologia
Armadilhas Extracelulares
Seres Humanos
Imunoglobulina G/análise
Peroxidase/análise
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Immunoglobulin G); 26NAK24LS8 (Hydralazine); EC 1.11.1.7 (Peroxidase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171004
[Lr] Data última revisão:
171004
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161018
[St] Status:MEDLINE
[do] DOI:10.1684/ejd.2016.2881


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[PMID]:27729205
[Au] Autor:Nishihara M; Takesue K; Hirooka Y
[Ad] Endereço:Department of Cardiovascular Medicine, Kyushu University Graduate School of Medical Sciences, Fukuoka, Japan.
[Ti] Título:Renal denervation enhances GABA-ergic input into the PVN leading to blood pressure lowering in chronic kidney disease.
[So] Source:Auton Neurosci;204:88-97, 2017 May.
[Is] ISSN:1872-7484
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Sympathoexcitation plays an important role in the pathogenesis of hypertension in patients with chronic kidney disease (CKD). The paraventricular nucleus of the hypothalamus (PVN) in the brain controls sympathetic outflow through γ-amino butyric acid (GABA)-ergic mechanisms. Renal denervation (RDN) exerts a long-term antihypertensive effect in hypertension with CKD; however, the effects of RDN on sympathetic nerve activity and GABA-ergic modulation in the PVN are not clear. We aimed to elucidate whether RDN modulates sympathetic outflow through GABA-ergic mechanisms in the PVN in hypertensive mice with CKD. METHODS AND RESULTS: In 5/6-nephrectomized male Institute of Cancer Research mice (Nx) at 4 weeks after nephrectomy, systolic blood pressure (SBP) was significantly increased, accompanied by sympathoexcitation. The Nx-mice underwent RDN or sham operation, and the mice were divided into three groups (Control, Nx-Sham, and Nx-RDN). At 2 weeks after RDN, SBP was significantly decreased and urinary sodium excretion was increased in Nx-RDN compared with Nx-Sham. Urinary norepinephrine excretion (uNE) levels did not differ significantly between Nx-RDN and Nx-Sham. At 6 weeks after RDN, SBP continued to decrease and uNE levels also decreased in Nx-RDN compared with Nx-Sham. Bicuculline microinjection into the PVN increased mean arterial pressure and lumbar sympathetic nerve activity in all groups. The pressor responses and change in lumbar sympathetic nerve activity were significantly attenuated in Nx-Sham, but were enhanced in Nx-RDN at 6 weeks after RDN. CONCLUSIONS: The findings from the present study indicate that RDN has a prolonged antihypertensive effect and, at least in the late phase, decreases sympathetic nerve activity in association with enhanced GABA-ergic input into the PVN in mice with CKD.
[Mh] Termos MeSH primário: Denervação
Neurônios GABAérgicos/fisiologia
Rim/inervação
Núcleo Hipotalâmico Paraventricular/cirurgia
Insuficiência Renal Crônica/cirurgia
[Mh] Termos MeSH secundário: Animais
Anti-Hipertensivos/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Pressão Sanguínea/fisiologia
Modelos Animais de Doenças
Ingestão de Alimentos/fisiologia
Hidralazina/farmacologia
Rim/efeitos dos fármacos
Rim/fisiopatologia
Rim/cirurgia
Masculino
Camundongos Endogâmicos ICR
Nefrectomia
Norepinefrina/urina
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Núcleo Hipotalâmico Paraventricular/fisiopatologia
Insuficiência Renal Crônica/tratamento farmacológico
Insuficiência Renal Crônica/fisiopatologia
Sistema Nervoso Simpático/efeitos dos fármacos
Sistema Nervoso Simpático/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 26NAK24LS8 (Hydralazine); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161013
[St] Status:MEDLINE



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