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[PMID]:28456475
[Au] Autor:Molinuevo MS; Fernández JM; Cortizo AM; McCarthy AD; Schurman L; Sedlinsky C
[Ad] Endereço:Laboratorio de Investigación en Osteopatías y Metabolismo Mineral, Facultad de Ciencias Exactas, Universidad Nacional de La Plata. 47 y 115, (1900) La Plata, Argentina.
[Ti] Título:Advanced glycation end products and strontium ranelate promote osteogenic differentiation of vascular smooth muscle cells in vitro: Preventive role of vitamin D.
[So] Source:Mol Cell Endocrinol;450:94-104, 2017 Jul 15.
[Is] ISSN:1872-8057
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Advanced glycation end products (AGE) have been demonstrated to induce the osteogenic trans-differentiation of vascular smooth muscle cells (VSMC). Strontium ranelate (SR) is an anti-osteoporotic agent that has both anti-catabolic and anabolic actions on bone tissue. However, in the last years SR has been associated with an increase of cardiovascular risk. We hypothesize that SR can increase the osteoblastic trans-differentiation of VSMC and the induction of extracellular calcifications, an effect that could be potentiated in the presence of AGE and inhibited by simultaneous administration of vitamin D. The present results of our in vitro experiments demonstrate that AGE and SR alone or in combination, stimulate L-type calcium channels, causing an increase in reactive oxygen species and activation of both ERK and NFkB, with the final effect of promoting the osteogenic shift of VSMC. Importantly, these in vitro effects of AGE and/or SR can be prevented by co-incubation with vitamin D.
[Mh] Termos MeSH primário: Diferenciação Celular/efeitos dos fármacos
Produtos Finais de Glicação Avançada/farmacologia
Músculo Liso Vascular/citologia
Miócitos de Músculo Liso/citologia
Osteogênese/efeitos dos fármacos
Tiofenos/farmacologia
Vitamina D/farmacologia
[Mh] Termos MeSH secundário: Animais
Ácido Ascórbico/farmacologia
Contagem de Células
Movimento Celular/efeitos dos fármacos
Subunidade alfa 1 de Fator de Ligação ao Core/metabolismo
Masculino
Modelos Biológicos
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/metabolismo
Nifedipino/farmacologia
Estresse Oxidativo/efeitos dos fármacos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Sulfassalazina/farmacologia
Vitamina E/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Core Binding Factor Alpha 1 Subunit); 0 (Glycation End Products, Advanced); 0 (Reactive Oxygen Species); 0 (Thiophenes); 04NQ160FRU (strontium ranelate); 1406-16-2 (Vitamin D); 1406-18-4 (Vitamin E); 3XC8GUZ6CB (Sulfasalazine); I9ZF7L6G2L (Nifedipine); PQ6CK8PD0R (Ascorbic Acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:28467360
[Au] Autor:Herzfeld E; Speh L; Strauss C; Scheller C
[Ad] Endereço:Department of Neurosurgery, Martin-Luther University of Halle-Wittenberg, Ernst-Grube-Str. 40, 06120 Halle (Saale), Germany. eva.herzfeld@uk-halle.de.
[Ti] Título:Nimodipine but Not Nifedipine Promotes Expression of Fatty Acid 2-Hydroxylase in a Surgical Stress Model Based on Neuro2a Cells.
[So] Source:Int J Mol Sci;18(5), 2017 May 03.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Nimodipine is well characterized for the management of aneurysmal subarachnoid hemorrhage and has been shown to promote a better outcome and less delayed ischemic neurological deficits. Animal and clinical trials show neuroprotective efficacy following nerve injuries. We showed a neuroprotective effect on Neuro2a cells. Subsequent microarray analysis revealed-among others-fatty acid 2-hydroxylase (FA2H) upregulated by nimodipine in vitro, which is a component of myelin synthesis. Differentiated Neuro2a cells were analyzed for nimodipine-mediated survival considering stress treatment in comparison to nifedipine-treatment. Cell survival was determined by measurement of LDH activity in the culture medium. Nimodipine decreased surgery-like stress-induced cell death of differentiated Neuro2a cells. Neuro2a cell culture was analyzed for changes in FA2H expression induced by nimodipine or nifedipine in surgery-like stress conditions. We analyzed expression levels of FA2H mRNA and protein by qPCR using specific primers or a FA2H-specific antibody in nimodipine or nifedipine non- and pre-treated Neuro2a cell culture, respectively. Nimodipine but not nifedipine increases FA2H protein levels and also significantly increases mRNA levels of FA2H in both undifferentiated and differentiated Neuro2a cells. Our findings indicate that higher expression of FA2H induced by nimodipine may cause higher survival of Neuro2a cells stressed with surgery-like stressors.
[Mh] Termos MeSH primário: Bloqueadores dos Canais de Cálcio/farmacologia
Resposta ao Choque Térmico/efeitos dos fármacos
Oxigenases de Função Mista/metabolismo
Fármacos Neuroprotetores/farmacologia
Procedimentos Neurocirúrgicos/efeitos adversos
Nifedipino/farmacologia
Nimodipino/farmacologia
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Morte Celular/efeitos dos fármacos
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Expressão Gênica
Camundongos
Oxigenases de Função Mista/genética
Bainha de Mielina/metabolismo
Nimodipino/uso terapêutico
RNA Mensageiro/genética
Estresse Mecânico
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Neuroprotective Agents); 0 (RNA, Messenger); 57WA9QZ5WH (Nimodipine); EC 1.- (Mixed Function Oxygenases); EC 1.- (fatty acid alpha-hydroxylase); I9ZF7L6G2L (Nifedipine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE


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[PMID]:29390463
[Au] Autor:Ng KK; Rozen G; Stewart T; Agresta F; Polyakov A
[Ad] Endereço:Melbourne Medical School, University of Melbourne.
[Ti] Título:A double-blinded, randomized, placebo-controlled trial assessing the effects of nifedipine on embryo transfer: Study protocol.
[So] Source:Medicine (Baltimore);96(51):e9194, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Implantation failure is the main factor affecting the success rate of in vitro fertilization (IVF) procedures. Studies have reported that uterine contractions (UCs) at the time of embryo transfer (ET) were inversely related to implantation and pregnancy rate, hence reducing the success of IVF treatment. Various pharmacological agents, with the exception of calcium channel blocker (CCB), have been investigated to reduce UC. In this regard, we are presenting a proposal for a double-blind randomized placebo-controlled trial. The trial aims to determine whether nifedipine, a CCB with potent smooth muscle relaxing activity and an excellent safety profile, can improve the outcome of ET. METHODS AND ANALYSES: We will recruit 100 infertile women into one of 2 groups: placebo (n = 50) and nifedipine 20 mg (n = 50). Study participants will be admitted 30 minutes prior to ET and given either tablet after their baseline vital signs have been recorded. They will then undergo ET and be observed for adverse events for another 30 minutes post-ET. The primary outcome will be implantation rate and clinical pregnancy rate. Secondary outcomes include adverse events, miscarriage and pregnancy, and neonatal outcomes. Resulting data will then be analyzed using t test, Chi-square test, and multivariate test to compare outcomes between the 2 groups for any statistical significance. This protocol has been designed in accordance with the SPIRIT 2013 Guidelines.
[Mh] Termos MeSH primário: Transferência Embrionária
Fertilização In Vitro/efeitos dos fármacos
Infertilidade Feminina/tratamento farmacológico
Nifedipino/administração & dosagem
Resultado da Gravidez
Taxa de Gravidez
[Mh] Termos MeSH secundário: Distribuição de Qui-Quadrado
Método Duplo-Cego
Feminino
Seres Humanos
Idade Materna
Análise Multivariada
Nifedipino/efeitos adversos
Gravidez
Medição de Risco
Tocolíticos/administração & dosagem
Tocolíticos/efeitos adversos
Vitória
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE I; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Tocolytic Agents); I9ZF7L6G2L (Nifedipine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009194


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[PMID]:29199222
[Au] Autor:Hosaka S; Tokunaga Y
[Ad] Endereço:Research and Development Division, Sawai Pharmaceutical Co., Ltd.
[Ti] Título:Differences in Powder Properties of Two 1,4-Dihydropyridine-Type Compounds Evaluated through Thermal Analysis.
[So] Source:Chem Pharm Bull (Tokyo);65(12):1175-1178, 2017.
[Is] ISSN:1347-5223
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The powder properties of two 1,4-dihydropyridine type compounds, manidipine dihydrochloride (Man) and benidipine hydrochloride (Ben), which possess similar physicochemical properties, were compared through thermal and mechanical analyses. Man and Ben were compressed with lactose monohydrate (Lac) and magnesium stearate (Mgst) at different compression forces. As an index, we focused on the onset temperatures of Lac dehydration during thermal analysis and plotted them against compression forces to evaluate the differences in powder properties between Man and Ben. To discuss in detail, the Lac ratio was selected as a formulation factor and compression speed as a process factor, which would be influenced to the onset temperature or its profile. It could be represented that Man was more adherent than Ben through thermal analysis by changing these critical factors, which were consistent with the results obtained through mechanical analysis.
[Mh] Termos MeSH primário: Di-Hidropiridinas/química
Nifedipino/análogos & derivados
[Mh] Termos MeSH secundário: Varredura Diferencial de Calorimetria
Força Compressiva
Lactose/química
Nifedipino/química
Ácidos Esteáricos/química
Comprimidos/química
Temperatura Ambiente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Dihydropyridines); 0 (Stearic Acids); 0 (Tablets); 0A6746FWDL (benidipine hydrochloride); 4ELV7Z65AP (stearic acid); 6O4754US88 (manidipine); I9ZF7L6G2L (Nifedipine); J2B2A4N98G (Lactose)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180110
[Lr] Data última revisão:
180110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.1248/cpb.c17-00375


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[PMID]:28068846
[Au] Autor:Haddad L; Corriveau S; Rousseau E; Blouin S; Pasquier JC; Ponsot Y; Roy-Lacroix MÈ
[Ad] Endereço:a Department of Obstetrics and Gynecology , Urology Division, Centre Hospitalier Universitaire de Sherbrooke , Sherbrooke , Québec , Canada.
[Ti] Título:Impact of tamsulosin and nifedipine on contractility of pregnant rat ureters in vitro .
[So] Source:J Matern Fetal Neonatal Med;31(2):191-196, 2018 Jan.
[Is] ISSN:1476-4954
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To evaluate the in vitro effect of tamsulosin and nifedipine on the contractility of pregnant rat ureters and to perform quantitative analysis of the pharmacological effects. Medical expulsive therapy (MET) is commonly used to treat urolithiasis. However, this treatment is seldom used in pregnant women since no studies support this practice. METHODS: This was an in vitro study on animal tissue derived from pregnant Sprague-Dawley rats. A total of 124 ureteral segments were mounted in an organ bath system and contractile response to methacholine (MCh) was assessed. Tamsulosin or nifedipine were added at cumulative concentrations (0.001-1 µM). The area under the curve (AUC) from isometric tension measurements was calculated. The effect of pharmacological agents and the respective controls were assessed by calculating the AUC for each 5-min interval. Statistical analyses were performed using the Mann-Whitney-Wilcoxon nonparametric test. RESULTS: Both drugs displayed statistically significant inhibitory activity at concentrations of 0.1 and 1 µM for tamsulosin and 1 µM for nifedipine when calculated as the AUC as compared to DMSO controls. CONCLUSION: Tamsulosin and nifedipine directly inhibit MCh-induced contractility of pregnant rat ureters. Further work is needed to determine the clinical efficacy of these medications for MET in pregnancy.
[Mh] Termos MeSH primário: Nifedipino/farmacologia
Sulfonamidas/farmacologia
Ureter/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Feminino
Cálculos Renais
Cloreto de Metacolina/farmacologia
Gravidez
Ratos
Ratos Sprague-Dawley
Ureter/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Sulfonamides); 0W5ETF9M2K (Methacholine Chloride); G3P28OML5I (tamsulosin); I9ZF7L6G2L (Nifedipine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170111
[St] Status:MEDLINE
[do] DOI:10.1080/14767058.2017.1280017


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[PMID]:28966136
[Au] Autor:Raheja R; Gupta H; Pandey U; Deshpande SB
[Ad] Endereço:Department of Physiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India.
[Ti] Título:Lignocaine augments the in-vitro uterine contractions involving NO-guanylyl cyclase dependent mechanisms.
[So] Source:Life Sci;190:52-57, 2017 Dec 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Lignocaine is used during intrapartum and postpartum period but there are conflicting reports regarding the effect of lignocaine on uterine contractility. Therefore, this study was undertaken to delineate the effect of lignocaine on uterine contractility and the underlying mechanisms. MAIN METHODS: The in vitro contractions were recorded from the uterine segments obtained from adult rats (in estrous phase) and also from human myometrial tissue. Effect of lignocaine on spontaneous uterine contractions was recorded in the absence or presence of antagonists. Effect of sodium nitroprusside (SNP, NO donor) on uterine contractility was assessed. The NO was assayed (indicator of NO activity) from the supernatant after exposing the myometrial tissue to lignocaine in the absence or the presence of L-NAME or hemoglobin. KEY FINDINGS: Lignocaine (100µM) increased the amplitude of uterine contractions by 75% with no alterations in frequency. Similar magnitude of increase was seen with human myometrial tissue also. The spontaneous activities were absent in Ca -free or in nifedipine (10µM) containing medium. Heparin (IP blocker, 10IU/ml), but not the indomethacin (10µM) blocked the lignocaine-induced augmentation. L-NAME (NOS inhibitor, 10µM) or methylene blue (guanylyl cyclase inhibitor, 100µM) partially blocked the lignocaine-induced augmentation. SNP (30µM) increased the amplitude of spontaneous uterine contractions. Lignocaine increased the NO content (indicator of NO activity) of uterine tissue and the increase was blocked by L-NAME or hemoglobin. SIGNIFICANCE: Present observations indicate that lignocaine augments the amplitude of uterine contractions via Ca -dependent mechanisms involving NO-G cyclase-dependent mechanisms.
[Mh] Termos MeSH primário: Anestésicos Locais/farmacologia
Guanilato Ciclase/metabolismo
Lidocaína/farmacologia
Óxido Nítrico/metabolismo
Contração Uterina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Feminino
Hemoglobinas/metabolismo
Seres Humanos
NG-Nitroarginina Metil Éster/farmacologia
Nifedipino/farmacologia
Nitroprussiato/farmacologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anesthetics, Local); 0 (Hemoglobins); 169D1260KM (Nitroprusside); 31C4KY9ESH (Nitric Oxide); 98PI200987 (Lidocaine); EC 4.6.1.2 (Guanylate Cyclase); I9ZF7L6G2L (Nifedipine); SY7Q814VUP (Calcium); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171003
[St] Status:MEDLINE


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[PMID]:28938466
[Au] Autor:Chimerel C; Riccio C; Murison K; Gribble FM; Reimann F
[Ad] Endereço:Metabolic Research Laboratories and Medical Research Council (MRC) Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Hospital, University of Cambridge, Cambridge CB2 0QQ, United Kingdom.
[Ti] Título:Optogenetic Analysis of Depolarization-Dependent Glucagonlike Peptide-1 Release.
[So] Source:Endocrinology;158(10):3426-3434, 2017 Oct 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Incretin hormones play an important role in the regulation of food intake and glucose homeostasis. Glucagonlike peptide-1 (GLP-1)-secreting cells have been demonstrated to be electrically excitable and to fire action potentials (APs) with increased frequency in response to nutrient exposure. However, nutrients can also be metabolized or activate G-protein-coupled receptors, thus potentially stimulating GLP-1 secretion independent of their effects on the plasma membrane potential. Here we used channelrhodopsins to manipulate the membrane potential of GLUTag cells, a well-established model of GLP-1-secreting enteroendocrine L cells. Using channelrhodopsins with fast or slow on/off kinetics (CheTA and SSFO, respectively), we found that trains of light pulses could trigger APs and calcium elevation in GLUTag cells stably expressing either CheTA or SSFO. Tetrodotoxin reduced light-triggered AP frequency but did not impair calcium responses, whereas further addition of the calcium-channel blockers nifedipine and ω-conotoxin GVIA abolished both APs and calcium transients. Light pulse trains did not trigger GLP-1 secretion from CheTA-expressing cells under basal conditions but were an effective stimulus when cyclic adenosine monophosphate (cAMP) concentrations were elevated by forskolin plus 3-isobutyl 1-methylxanthine. In SSFO-expressing cells, light-stimulated GLP-1 release was observed at resting and elevated cAMP concentrations and was blocked by nifedipine plus ω-conotoxin GVIA but not tetrodotoxin. We conclude that cAMP elevation or cumulative membrane depolarization triggered by SSFO enhances the efficiency of light-triggered action potential firing, voltage-gated calcium entry, and GLP-1 secretion.
[Mh] Termos MeSH primário: Potenciais de Ação/efeitos dos fármacos
Bloqueadores dos Canais de Cálcio/farmacologia
Células Enteroendócrinas/efeitos dos fármacos
Peptídeo 1 Semelhante ao Glucagon/efeitos dos fármacos
Potenciais da Membrana/efeitos dos fármacos
[Mh] Termos MeSH secundário: 1-Metil-3-Isobutilxantina/farmacologia
Animais
Cálcio/metabolismo
Colforsina/farmacologia
Células Enteroendócrinas/metabolismo
Células Enteroendócrinas/secreção
Peptídeo 1 Semelhante ao Glucagon/secreção
Camundongos
Nifedipino/farmacologia
Optogenética
Técnicas de Patch-Clamp
Inibidores de Fosfodiesterase/farmacologia
Rodopsina
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
Vasodilatadores/farmacologia
ômega-Conotoxina GVIA/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Phosphodiesterase Inhibitors); 0 (Sodium Channel Blockers); 0 (Vasodilator Agents); 1F7A44V6OU (Colforsin); 4368-28-9 (Tetrodotoxin); 89750-14-1 (Glucagon-Like Peptide 1); 9009-81-8 (Rhodopsin); 92078-76-7 (omega-Conotoxin GVIA); I9ZF7L6G2L (Nifedipine); SY7Q814VUP (Calcium); TBT296U68M (1-Methyl-3-isobutylxanthine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00434


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[PMID]:28899749
[Au] Autor:Hammoud SH; Omar AG; Eid AA; El-Mas MM
[Ad] Endereço:Department of Pharmacology and Therapeutics, Faculty of Pharmacy, Beirut Arab University, Lebanon.
[Ti] Título:CYP4A/CYP2C modulation of the interaction of calcium channel blockers with cyclosporine on EDHF-mediated renal vasodilations in rats.
[So] Source:Toxicol Appl Pharmacol;334:110-119, 2017 Nov 01.
[Is] ISSN:1096-0333
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The endothelium-derived hyperpolarizing factor (EDHF) serves as a back-up mechanism that compensates for reduced nitric oxide (NO)/prostanoids bioavailability. Here we investigated whether (i) under conditions of vascular endothelium dysfunction, the immunosuppressant drug cyclosporine (CSA) upregulates EDHF-dependent renal vasodilations through altering CYP4A/CYP2C signaling, and (ii) calcium channel blockers modulate the CSA/EDHF/CYP interaction. Rats were treated with CSA, verapamil, nifedipine, or their combinations for 7days. Blood pressure (BP) was measured by tail-cuff plethysmography. Kidneys were then isolated, perfused with physiological solution containing L-NAME (NOS inhibitor) and diclofenac (cyclooxygenase inhibitor, DIC), and preconstricted with phenylephrine. CSA (25mgkg day for 7days) increased BP and augmented carbachol renal vasodilations. The co-treatment with verapamil (2mgkg day ) or nifedipine (3mgkg day ) abolished CSA hypertension and conversely affected carbachol vasodilations (increases vs. decreases). Infusion of MSPPOH (epoxyeicosatrienoic acids, EETs, inhibitor) reduced carbachol vasodilations in kidneys of all rat groups, suggesting the importance of EETs in these responses. By contrast, 20-Hydroxyeicosatetraenoic Acid (20-HETE) inhibition by HET0016 increased carbachol vasodilations in control rats, an effect that disappeared by CSA treatment, and reappeared in rats treated with CSA/verapamil or CSA/nifedipine. Renal protein expression of CYP2C and CYP4A as well as their vasoactive products (EETs/20-HETE) were increased in CSA-treated rats. Whereas the CYP2C/EETs effects of CSA were abolished by verapamil and intensified by nifedipine, the CYP4A/20-HETE effects were reduced by either CCB. Overall, nifedipine and verapamil blunts CSA hypertension but variably affected concomitantly enhanced EDHF-dependent renal vasodilations and alterations in CYP2C/CYP4A signaling.
[Mh] Termos MeSH primário: Fatores Biológicos/metabolismo
Bloqueadores dos Canais de Cálcio/farmacologia
Ciclosporina/farmacologia
Citocromo P-450 CYP4A/metabolismo
Sistema Enzimático do Citocromo P-450/metabolismo
Imunossupressores/farmacologia
[Mh] Termos MeSH secundário: Animais
Bloqueadores dos Canais de Cálcio/administração & dosagem
Ciclosporina/administração & dosagem
Citocromo P-450 CYP4A/genética
Sistema Enzimático do Citocromo P-450/genética
Interações Medicamentosas
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Imunossupressores/administração & dosagem
Rim/irrigação sanguínea
Masculino
Nifedipino/administração & dosagem
Nifedipino/farmacologia
Ratos
Ratos Sprague-Dawley
Vasodilatação/efeitos dos fármacos
Verapamil/administração & dosagem
Verapamil/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biological Factors); 0 (Calcium Channel Blockers); 0 (Immunosuppressive Agents); 0 (cytochrome P-450 CYP2C subfamily); 0 (endothelium-dependent hyperpolarization factor); 83HN0GTJ6D (Cyclosporine); 9035-51-2 (Cytochrome P-450 Enzyme System); CJ0O37KU29 (Verapamil); EC 1.14.15.3 (Cytochrome P-450 CYP4A); I9ZF7L6G2L (Nifedipine)
[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:170914
[St] Status:MEDLINE


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[PMID]:28893900
[Au] Autor:Webster LM; Myers JE; Nelson-Piercy C; Harding K; Cruickshank JK; Watt-Coote I; Khalil A; Wiesender C; Seed PT; Chappell LC
[Ad] Endereço:From the Women's Health Academic Centre, King's College London, United Kingdom (L.M.W., C.N.-P., P.T.S., L.C.C.); Directorate of Women's Health, Guy's and St Thomas' Foundation Trust, London, United Kingdom (L.M.W., C.N.-P., K.H., L.C.C.); Maternaland Fetal Health ResearchCenter, Division of Develop
[Ti] Título:Labetalol Versus Nifedipine as Antihypertensive Treatment for Chronic Hypertension in Pregnancy: A Randomized Controlled Trial.
[So] Source:Hypertension;70(5):915-922, 2017 Nov.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Data from randomized controlled trials to guide antihypertensive agent choice for chronic hypertension in pregnancy are limited; this study aimed to compare labetalol and nifedipine, additionally assessing the impact of ethnicity on treatment efficacy. Pregnant women with chronic hypertension (12 -27 weeks' gestation) were enrolled at 4 UK centers (August 2014 to October 2015). Open-label first-line antihypertensive treatment was randomly assigned: labetalol- (200-1800 mg/d) or nifedipine-modified release (20-80 mg/d). Analysis included 112 women (98%) who completed the study (labetalol n=55, nifedipine n=57). Maximum blood pressure after randomization was 161/101 mm Hg with labetalol versus 163/105 mm Hg with nifedipine (mean difference systolic: 1.2 mm Hg [-4.9 to 7.2 mm Hg], diastolic: 3.3 mm Hg [-0.6 to 7.3 mm Hg]). Mean blood pressure was 134/84 mm Hg with labetalol and 134/85 mm Hg with nifedipine (mean difference systolic: 0.3 mm Hg [-2.8 to 3.4 mm Hg], and diastolic: -1.9 mm Hg [-4.1 to 0.3 mm Hg]). Nifedipine use was associated with a 7.4-mm Hg reduction (-14.4 to -0.4 mm Hg) in central aortic pressure, measured by pulse wave analysis. No difference in treatment effect was observed in black women (n=63), but a mean 4 mm Hg reduction (-6.6 to -0.8 mm Hg; =0.015) in brachial diastolic blood pressure was observed with labetalol compared with nifedipine in non-black women (n=49). Labetalol and nifedipine control mean blood pressure to target in pregnant women with chronic hypertension. This study provides support for a larger definitive trial scrutinizing the benefits and side effects of first-line antihypertensive treatment. CLINICAL TRIAL REGISTRATION: URL: https://www.isrctn.com. Unique identifier: ISRCTN40973936.
[Mh] Termos MeSH primário: Pressão Arterial/efeitos dos fármacos
Hipertensão
Labetalol
Nifedipino
Complicações Cardiovasculares na Gravidez
[Mh] Termos MeSH secundário: Adulto
Anti-Hipertensivos/administração & dosagem
Anti-Hipertensivos/efeitos adversos
Determinação da Pressão Arterial/métodos
Monitoramento de Medicamentos/métodos
Feminino
Idade Gestacional
Seres Humanos
Hipertensão/diagnóstico
Hipertensão/tratamento farmacológico
Labetalol/administração & dosagem
Labetalol/efeitos adversos
Nifedipino/administração & dosagem
Nifedipino/efeitos adversos
Gravidez
Complicações Cardiovasculares na Gravidez/diagnóstico
Complicações Cardiovasculares na Gravidez/tratamento farmacológico
Análise de Onda de Pulso/métodos
Resultado do Tratamento
Reino Unido
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Antihypertensive Agents); I9ZF7L6G2L (Nifedipine); R5H8897N95 (Labetalol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09972


  10 / 15288 MEDLINE  
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[PMID]:28855109
[Au] Autor:Li H; Kim HW; Shin SE; Seo MS; An JR; Ha KS; Han ET; Hong SH; Firth AL; Choi IW; Han IY; Lee DS; Yim MJ; Park WS
[Ad] Endereço:Department of Physiology, Kangwon National University School of Medicine, Chuncheon 24341, South Korea.
[Ti] Título:The vasorelaxant effect of mitiglinide via activation of voltage-dependent K channels and SERCA pump in aortic smooth muscle.
[So] Source:Life Sci;188:1-9, 2017 Nov 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: The vasorelaxant effects of the anti-diabetic drug, mitiglinide in phenylephrine (Phe)-pre-contracted aortic rings were examined. MATERIALS AND METHODS: Arterial tone measurement was performed in aortic smooth muscle cells. KEY FINDINGS: Mitiglinide dose-dependently induced vasorelaxation. Application of the large-conductance Ca -activated K (BK ) channel blocker paxilline, inwardly rectifying K (Kir) channel blocker Ba , and ATP-sensitive K (K ) channel blocker glibenclamide did not affect the vasorelaxant effect of mitiglinide. However, application of the voltage-dependent K (Kv) channel blocker 4-AP, effectively inhibited mitiglinide-induced vasorelaxation. Although pretreatment with the Ca channel blocker nifedipine did not alter the mitiglinide-induced vasorelaxation, pretreatment with the sarcoplasmic/endoplasmic reticulum Ca -ATPase (SERCA) pump inhibitor thapsigargin and cyclopiazonic acid reduced the vasorelaxant effect of mitiglinide. In addition, the vasorelaxant effect of mitiglinide was not affected by the inhibitors of adenylyl cyclase, protein kinase A, guanylyl cyclase, or protein kinase G. Elimination of the endothelium and inhibition of endothelium-dependent vasorelaxant mechanisms also did not change the vasorelaxant effect of mitiglinide. SIGNIFICANCE: We proposed that mitiglinide induces vasorelaxation via activation of Kv channels and SERCA pump. However, the vasorelaxant effects of mitiglinide did not involve other K channels, Ca channels, PKA/PKG signaling pathways, or the endothelium.
[Mh] Termos MeSH primário: Aorta Torácica/fisiologia
Isoindóis/farmacologia
Músculo Liso/fisiologia
Canais de Potássio de Abertura Dependente da Tensão da Membrana/agonistas
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/fisiologia
Vasodilatadores/farmacologia
[Mh] Termos MeSH secundário: 4-Aminopiridina/farmacologia
Adenina/análogos & derivados
Adenina/farmacologia
Animais
Aorta Torácica/efeitos dos fármacos
Bário/farmacologia
Carbazóis/farmacologia
Relação Dose-Resposta a Droga
Interações Medicamentosas
Endotélio Vascular/efeitos dos fármacos
Glibureto/farmacologia
Indóis/farmacologia
Isoindóis/antagonistas & inibidores
Masculino
Músculo Liso/efeitos dos fármacos
Nifedipino/farmacologia
Oxidiazóis/farmacologia
Fenilefrina/farmacologia
Pirróis/farmacologia
Quinoxalinas/farmacologia
Coelhos
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Tapsigargina/farmacologia
Vasodilatadores/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one); 0 (Carbazoles); 0 (Indoles); 0 (Isoindoles); 0 (Oxadiazoles); 0 (Potassium Channels, Voltage-Gated); 0 (Pyrroles); 0 (Quinoxalines); 0 (Vasodilator Agents); 126643-37-6 (KT 5823); 17318-31-9 (9-(tetrahydro-2-furyl)-adenine); 1WS297W6MV (Phenylephrine); 24GP945V5T (Barium); 3T9U9Z96L7 (paxilline); 58HV29I28S (KT 5720); 67526-95-8 (Thapsigargin); BH3B64OKL9 (4-Aminopyridine); D86I0XLB13 (mitiglinide); EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases); I9ZF7L6G2L (Nifedipine); JAC85A2161 (Adenine); SX6K58TVWC (Glyburide); X9TLY4580Z (cyclopiazonic acid)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE



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