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[PMID]:29215340
[Au] Autor:Yakut K; Erdogan I; Varan B; Atar I
[Ad] Endereço:Department of Pediatric Cardiology, Baskent University Ankara Hospital, Ankara, Turkey.
[Ti] Título:A Report of Brugada Syndrome Presenting with Cardiac Arrest Triggered by Verapamil Intoxication.
[So] Source:Balkan Med J;34(6):576-579, 2017 12 01.
[Is] ISSN:2146-3131
[Cp] País de publicação:Turkey
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Brugada syndrome is a disease characterized by a specific electrocardiographic pattern and an increased risk of sudden cardiac death. We present this case with the updated literature to emphasise the need to consider the diagnosis of Brugada syndrome in patients admitted to the emergency ward with sudden cardiac arrest. CASE REPORT: A 16-year-old female patient was admitted to the emergency ward with complaints of weakness and abdominal pain, and she had four cardiac arrests during her evaluation period. She was referred to our clinic for permanent pacemaker implantation. She was on a temporary pace maker after having had C-reactive protein. Her physical exam was normal except for bilaterally decreased lung sounds. Lung x-ray and computed tomography, which were performed by another institution, revealed minimal pleural effusion and nothing else of significance. Blood and peritoneal fluid samples were sterile. Echocardiographic exam and cardiac enzymes were also in the normal ranges. Electrocardiographic showed incomplete right branch block in leads V1 and V2. An ajmaline test revealed specific electrocardiographic findings of the type I Brugada pattern. We proposed implanting an implantable cardioverter defibrillator to the patient as there were positive findings on the ajmaline test as well as a history of sudden cardiac arrest. After this treatment proposal, the patient's family admitted that she had taken a high dose of verapamil and thus, the encountered bradycardia was associated with verapamil overuse. The ajmaline test was repeated as it was contemplated that the previous positive ajmaline test had been associated with verapamil overuse. Implantable cardioverter defibrillator implantation was proposed again as there was a history of sudden cardiac arrest; however, the family did not consent to implantable cardioverter defibrillator, and the patient was discharged and followed up. CONCLUSION: Brugada syndrome should be considered for patients who are admitted to the emergency ward with sudden cardiac arrest though surface electrocardiographic is normal. If there is a suspicion of Brugada syndrome, repeated electrocardiographic should be performed on different occasions. Diagnosis can be clarified by upper costal electrocardiographic or by administering Na channel blockers during electrocardiographic performance.
[Mh] Termos MeSH primário: Antiarrítmicos/envenenamento
Síndrome de Brugada/induzido quimicamente
Parada Cardíaca/induzido quimicamente
Verapamil/envenenamento
[Mh] Termos MeSH secundário: Adolescente
Ajmalina/farmacologia
Síndrome de Brugada/diagnóstico
Síndrome de Brugada/fisiopatologia
Diagnóstico Diferencial
Eletrocardiografia
Feminino
Testes Genéticos
Parada Cardíaca/fisiopatologia
Seres Humanos
Fatores Desencadeantes
Bloqueadores dos Canais de Sódio/administração & dosagem
Tentativa de Suicídio
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Sodium Channel Blockers); 1PON08459R (Ajmaline); CJ0O37KU29 (Verapamil)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE
[do] DOI:10.4274/balkanmedj.2016.1301


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[PMID]:29307525
[Au] Autor:Candenas L; Pinto FM; Cejudo-Román A; González-Ravina C; Fernández-Sánchez M; Pérez-Hernández N; Irazusta J; Subirán N
[Ad] Endereço:Instituto de Investigaciones Químicas (L.C., F.M.P., A.C.-R., N.P.), CSIC, Seville, Spain. Electronic address: luzcandenas@iiq.csic.es.
[Ti] Título:Veratridine-sensitive Na channels regulate human sperm fertilization capacity.
[So] Source:Life Sci;196:48-55, 2018 Mar 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: The sperm plasma membrane contains specific ion channels and transporters that initiate changes in Ca , Na , K and H ions in the sperm cytoplasm. Ion channels are key regulators of the sperm membrane potential, cytoplasmic Ca and intracellular pH (pH ), which leads to regulate motility, capacitation, acrosome reaction and other physiological processes crucial for successful fertilization. Expression of epithelial sodium channels (ENaC) and voltage-gated sodium channels (Na ) in human spermatozoa has been reported, but the role of Na fluxes sodium channels in the regulation of sperm cell function remains poorly understood. In this context, we aimed to analyze the physiological role of Na channels in human sperm. MAIN METHODS: Motility and hyperactivation analysis was conducted by CASA analysis. Flow cytometry and spectrophotometry approaches were carried out to measure Capacitation, Acrosome reaction, immunohistochemistry for Tyr-residues phosporylation, [Ca ] levels and membrane potential. KEY FINDINGS: Functional studies showed that veratridine, a voltage-gated sodium channel activator, increased sperm progressive motility without producing hyperactivation while the Na antagonist lidocaine did induce hyperactivated motility. Veratridine increased protein tyrosine phosphorylation, an event occurring during capacitation, and its effects were inhibited in the presence of lidocaine and tetrodotoxin. Veratridine had no effect on the acrosome reaction by itself, but was able to block the progesterone-induced acrosome reaction. Moreover, veratridine caused a membrane depolarization and modified the effect of progesterone on [Ca ] and sperm membrane potential. SIGNIFICANCE: Our results suggest that veratridine-sensitive Na channels are involved on human sperm fertility acquisition regulating motility, capacitation and the progesterone-induced acrosome reaction in human sperm.
[Mh] Termos MeSH primário: Fertilização/efeitos dos fármacos
Agonistas de Canais de Sódio/farmacologia
Canais de Sódio/efeitos dos fármacos
Espermatozoides/efeitos dos fármacos
Veratridina/farmacologia
[Mh] Termos MeSH secundário: Reação Acrossômica/efeitos dos fármacos
Adolescente
Adulto
Feminino
Seres Humanos
Imuno-Histoquímica
Técnicas In Vitro
Lidocaína/farmacologia
Masculino
Potenciais da Membrana/efeitos dos fármacos
Progesterona/antagonistas & inibidores
Progesterona/farmacologia
Receptores Androgênicos/efeitos dos fármacos
Sêmen/efeitos dos fármacos
Sódio/metabolismo
Bloqueadores dos Canais de Sódio/farmacologia
Capacitação Espermática/efeitos dos fármacos
Motilidade Espermática/efeitos dos fármacos
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Androgen); 0 (Sodium Channel Agonists); 0 (Sodium Channel Blockers); 0 (Sodium Channels); 4G7DS2Q64Y (Progesterone); 71-62-5 (Veratridine); 98PI200987 (Lidocaine); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


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[PMID]:29247746
[Au] Autor:Sun X; Tang L; Winesett S; Chang W; Cheng SX
[Ad] Endereço:Department of Physiology and Pathophysiology, School of Basic Medicine, Qingdao University, Qingdao, China; Department of Pediatrics, University of Florida, Gainesville, FL, USA.
[Ti] Título:Calcimimetic R568 inhibits tetrodotoxin-sensitive colonic electrolyte secretion and reduces c-fos expression in myenteric neurons.
[So] Source:Life Sci;194:49-58, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Calcium-sensing receptor (CaSR) is expressed on neurons of both submucosal and myenteric plexuses of the enteric nervous system (ENS) and the CaSR agonist R568 inhibited Cl secretion in intestine. The purpose of this study was to localize the primary site of action of R568 in the ENS and to explore how CaSR regulates secretion through the ENS. MATERIALS AND METHODS: Two preparations of rat proximal and distal colon were used. The full-thickness preparation contained both the submucosal and myenteric plexuses, whereas for the "stripped" preparation the myenteric plexus with the muscle layers was removed. Both preparations were mounted onto Ussing chambers and Cl secretory responses were compared by measuring changes in short circuit current (I ). Two tissue-specific CaSR knockouts (i.e., neuron-specific vs. enterocyte-specific) were generated to compare the effect of R568 on expression of c-fos protein in myenteric neurons by immunocytochemistry. KEY FINDINGS: In full-thickness colons, tetrodotoxin (TTX) inhibited I , both in proximal and distal colons. A nearly identical inhibition was produced by R568. However, in stripped preparations, while the effect of TTX on I largely remained, the effect of R568 was nearly completely eliminated. In keeping with this, R568 reduced c-fos protein expression only in myenteric neurons of wild type mice and mutant mice that contained CaSR in neurons (i.e., Cre/Casr mice), but not in myenteric neurons of Cre/Casr mice in which neuronal cell CaSR was eliminated. SIGNIFICANCE: These results indicate that R568 exerts its anti-secretory effects predominantly via CaSR-mediated inhibition of neuronal activity in the myenteric plexus.
[Mh] Termos MeSH primário: Eletrólitos/metabolismo
Plexo Mientérico/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Fenetilaminas/farmacologia
Propilaminas/farmacologia
Proteínas Proto-Oncogênicas c-fos/metabolismo
Receptores de Detecção de Cálcio/metabolismo
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
[Mh] Termos MeSH secundário: Animais
Colo/efeitos dos fármacos
Colo/metabolismo
Masculino
Camundongos Endogâmicos C57BL
Plexo Mientérico/citologia
Neurônios/metabolismo
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Electrolytes); 0 (N-(2-chlorophenylpropyl)-1-(3-methoxyphenyl)ethylamine); 0 (Phenethylamines); 0 (Propylamines); 0 (Proto-Oncogene Proteins c-fos); 0 (Receptors, Calcium-Sensing); 0 (Sodium Channel Blockers); 4368-28-9 (Tetrodotoxin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171217
[St] Status:MEDLINE


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[PMID]:28452816
[Au] Autor:Santamaria CM; Zhan C; McAlvin JB; Zurakowski D; Kohane DS
[Ad] Endereço:From the *Laboratory for Biomaterials and Drug Delivery, Division of Critical Care Medicine, Department of Anesthesiology; †Division of Medicine Critical Care, Department of Medicine; and ‡Department of Anesthesiology, Perioperative, and Pain Medicine, Boston Children's Hospital, Boston, Massachusetts.
[Ti] Título:Tetrodotoxin, Epinephrine, and Chemical Permeation Enhancer Combinations in Peripheral Nerve Blockade.
[So] Source:Anesth Analg;124(6):1804-1812, 2017 06.
[Is] ISSN:1526-7598
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Chemical permeation enhancers (CPEs) have the potential to improve nerve blockade by site 1 sodium channel blockers such as tetrodotoxin (TTX). Here, we investigated the efficacy and toxicity of CPE-enhanced nerve blockade across a range of TTX concentrations using 2 CPEs (sodium octyl sulfate and octyl trimethyl ammonium bromide). We also tested the hypothesis that CPEs could be used to reduce the concentrations of TTX and/or of a second adjuvant drug (in this case, epinephrine) needed to achieve prolonged local anesthesia METHODS:: Sprague-Dawley rats were injected at the sciatic nerve with combinations of TTX and CPEs, with and without epinephrine. Sensory and motor nerve blockade were assessed using a modified hot plate test and a weight-bearing test, respectively. Systemic and local toxicities of the different combinations were assessed. RESULTS: Addition of increasing concentrations of TTX to fixed concentrations of CPEs produced a marked concentration-dependent improvement in the rate of successful nerve blocks and in nerve block duration. CPEs did not affect systemic toxicity. At some concentrations, the addition of sodium octyl sulfate increased the duration of block from TTX plus epinephrine, and epinephrine increased that from TTX plus CPEs. The addition of epinephrine did not cause an increase in local toxicity, and it markedly reduced systemic toxicity. CONCLUSIONS: CPEs can prolong the duration of nerve blockade across a range of concentrations of TTX. CPEs could also be used to reduce the concentration of epinephrine needed to achieve a given degree of nerve block. CPEs may be useful in enhancing nerve blockade from site 1 sodium channel blockers.
[Mh] Termos MeSH primário: Agonistas Adrenérgicos/farmacologia
Ácidos Alcanossulfônicos/farmacologia
Anestésicos Locais/farmacologia
Epinefrina/farmacologia
Bloqueio Nervoso/métodos
Compostos de Amônio Quaternário/farmacologia
Nervo Isquiático/efeitos dos fármacos
Bloqueadores dos Canais de Sódio/farmacologia
Tetrodotoxina/farmacologia
[Mh] Termos MeSH secundário: Agonistas Adrenérgicos/toxicidade
Anestésicos Locais/toxicidade
Animais
Difusão
Relação Dose-Resposta a Droga
Epinefrina/toxicidade
Masculino
Atividade Motora/efeitos dos fármacos
Bloqueio Nervoso/efeitos adversos
Limiar da Dor/efeitos dos fármacos
Permeabilidade
Ratos Sprague-Dawley
Bloqueadores dos Canais de Sódio/toxicidade
Tetrodotoxina/toxicidade
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Adrenergic Agonists); 0 (Alkanesulfonic Acids); 0 (Anesthetics, Local); 0 (Quaternary Ammonium Compounds); 0 (Sodium Channel Blockers); 15461-38-8 (octyltrimethylammonium); 4368-28-9 (Tetrodotoxin); DU4821I15A (1-octanesulfonic acid); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1213/ANE.0000000000002072


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[PMID]:28455610
[Au] Autor:Bengel P; Ahmad S; Sossalla S
[Ad] Endereço:Clinic for Cardiology and Pneumology/Heart Center, University Medical Center Goettingen, DZHK (German Centre for Cardiovascular Research), Goettingen, Germany.
[Ti] Título:Inhibition of Late Sodium Current as an Innovative Antiarrhythmic Strategy.
[So] Source:Curr Heart Fail Rep;14(3):179-186, 2017 Jun.
[Is] ISSN:1546-9549
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE OF REVIEW: Over the last years, evidence is accumulating that enhanced late sodium current (I ) in cardiac pathologies has fundamental consequences for cellular electrophysiology. This review discusses the underlying mechanisms of I -induced arrhythmias and the significance of I -inhibition as a possible therapeutic approach. RECENT FINDINGS: Inhibition of enhanced I , e.g., by ranolazine, was shown to reverse these effects in different myocardial diseases including heart failure. The antianginal drug ranolazine has already been examined in larger clinical trials with promising antiarrhythmic actions. Enhanced I was found to be present in several cardiac pathologies like ischemia, long QT syndromes, hypertrophic cardiomyopathy, and heart failure. In settings of enhanced I , a sodium-dependent calcium overload leads to severe impairment of excitation-contraction coupling and therefore has a high proarrhythmogenic potential. Experimental data showed that inhibition of I has a high antiarrhythmic potential which could be confirmed in further clinical trials.
[Mh] Termos MeSH primário: Antiarrítmicos/uso terapêutico
Arritmias Cardíacas/tratamento farmacológico
Ranolazina/uso terapêutico
Bloqueadores dos Canais de Sódio/uso terapêutico
Canais de Sódio/efeitos dos fármacos
[Mh] Termos MeSH secundário: Arritmias Cardíacas/etiologia
Insuficiência Cardíaca/tratamento farmacológico
Insuficiência Cardíaca/metabolismo
Seres Humanos
Síndrome do QT Longo/metabolismo
Canais de Sódio/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Sodium Channel Blockers); 0 (Sodium Channels); A6IEZ5M406 (Ranolazine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1007/s11897-017-0333-0


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[PMID]:29046002
[Au] Autor:Ong P; Sechtem U
[Ti] Título:[Optimal Diagnostics and Therapy for Microvascular Angina Pectoris].
[Ti] Título:Optimale Diagnostik und Therapie der mikrovaskulären Angina pectoris..
[So] Source:Dtsch Med Wochenschr;142(21):1586-1593, 2017 Oct.
[Is] ISSN:1439-4413
[Cp] País de publicação:Germany
[La] Idioma:ger
[Ab] Resumo:Patients with microvascular angina are characterized by angina pectoris with proof of myocardial ischemia in the absence of any relevant epicardial stenosis and without myocardial disease (type 1 coronary microvascular dysfunction according to Crea and Camici). Structural and functional alterations of the coronary microvessels (diameter < 500 µm) are the reason for this phenomenon. Frequently such alterations are associated with cardiovascular risk factors. Patients with angina pectoris without epicardial stenoses represent for 10 - 50 % of all patients undergoing coronary angiography depending on the clinical presentation. Diagnostic approaches include non-invasive (e. g. combination of coronary CT-angiography and positron emission tomography/echo Doppler-based coronary flow reserve measurements) as well as invasive procedures (coronary flow reserve measurements in response to adenosine, intracoronary acetylcholine testing). Pharmacological treatment of these patients is often challenging and should be based on the characterization of the underlying mechanisms. Moreover, strict risk factor control and individually titrated combinations of antianginal substances (e. g. beta blockers, calcium channel blockers, nitrates, ranolazine, ivabradine etc.) are recommended.
[Mh] Termos MeSH primário: Angina Microvascular/diagnóstico
Angina Microvascular/terapia
[Mh] Termos MeSH secundário: Antagonistas Adrenérgicos beta/uso terapêutico
Bloqueadores dos Canais de Cálcio/uso terapêutico
Fármacos Cardiovasculares/uso terapêutico
Vasoespasmo Coronário/complicações
Vasos Coronários/fisiopatologia
Seres Humanos
Neuroestimuladores Implantáveis
Angina Microvascular/fisiopatologia
Isquemia Miocárdica/complicações
Condicionamento Físico Humano
Fatores de Risco
Bloqueadores dos Canais de Sódio/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Calcium Channel Blockers); 0 (Cardiovascular Agents); 0 (Sodium Channel Blockers)
[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:171019
[St] Status:MEDLINE
[do] DOI:10.1055/s-0043-104469


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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]:28739252
[Au] Autor:Szulczyk B; Nurowska E
[Ad] Endereço:Department of Drug Technology and Pharmaceutical Biotechnology, The Medical University of Warsaw, Banacha 1, 02-097, Poland. Electronic address: bartlomiej.szulczyk@wum.edu.pl.
[Ti] Título:Valproic acid inhibits TTX-resistant sodium currents in prefrontal cortex pyramidal neurons.
[So] Source:Biochem Biophys Res Commun;491(2):291-295, 2017 Sep 16.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Valproic acid is frequently prescribed and used to treat epilepsy, bipolar disorder and other conditions. However, the mechanism of action of valproic acid has not been fully elucidated. The aim of this study was to assess the influence of valproic acid (200 µM) on TTX-resistant sodium currents in mPFC pyramidal neurons. Valproic acid inhibited the maximal amplitude and did not change the activation parameters of TTX-resistant sodium currents. Moreover, valproic acid (2 µM and 200 µM) shifted the TTX-resistant sodium channel inactivation curve towards hyperpolarisation. In the presence of valproic acid, TTX-resistant sodium currents recovered from inactivation more slowly. Valproic acid did not influence the use-dependent blockade of TTX-resistant sodium currents. This study suggests that a potential new mechanism of the antiepileptic action of valproic acid is, among others, inhibition of TTX-resistant sodium currents.
[Mh] Termos MeSH primário: Anticonvulsivantes/farmacologia
Células Piramidais/efeitos dos fármacos
Bloqueadores dos Canais de Sódio/farmacologia
Canais de Sódio/metabolismo
Tetrodotoxina/farmacologia
Ácido Valproico/farmacologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/fisiologia
Animais
Técnicas de Cultura de Células
Microtomia
Técnicas de Patch-Clamp
Córtex Pré-Frontal/citologia
Córtex Pré-Frontal/efeitos dos fármacos
Córtex Pré-Frontal/metabolismo
Cultura Primária de Células
Células Piramidais/citologia
Células Piramidais/metabolismo
Ratos
Sódio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticonvulsants); 0 (Sodium Channel Blockers); 0 (Sodium Channels); 4368-28-9 (Tetrodotoxin); 614OI1Z5WI (Valproic Acid); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170824
[Lr] Data última revisão:
170824
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE


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[PMID]:28704809
[Au] Autor:Stagno MJ; Zacharopoulou N; Bochem J; Tsapara A; Pelzl L; Al-Maghout T; Kallergi G; Alkahtani S; Alevizopoulos K; Dimas K; Calogeropoulou T; Warmann SW; Lang F; Schmid E; Stournaras C
[Ad] Endereço:Department of Pediatric Surgery & Pediatric Urology, Children's Hospital, Eberhard-Karls-University Tuebingen, Tuebingen, Germany.
[Ti] Título:Istaroxime Inhibits Motility and Down-Regulates Orai1 Expression, SOCE and FAK Phosphorylation in Prostate Cancer Cells.
[So] Source:Cell Physiol Biochem;42(4):1366-1376, 2017.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Istaroxime is a validated inotropic Na+/K+ ATPase inhibitor currently in development for the treatment of various cardiac conditions. Recent findings established that this steroidal drug exhibits potent apoptotic responses in prostate tumors in vitro and in vivo, by affecting key signaling orchestrating proliferation and apoptosis, such as c-Myc and caspase 3, Rho GTPases and actin cytoskeleton dynamics. In the present study we examined whether istaroxime is affecting cell motility and analyzed the underlying mechanism in prostate tumor cells. METHODS: Migration was assessed by transwell and wound healing assays, Orai1 and Stim1 abundance by RT-PCR and confocal immunofluorescence microscopy, Fura-2 fluorescence was utilized to determine intracellular Ca2+ and Western blotting for FAK/pFAK measurements. RESULTS: We observed strong inhibition of cell migration in istaroxime treated DU-145 prostate cancer cells. Istaroxime further decreased Orai1 and Stim1 transcript levels and downregulated Orai1 protein expression. Moreover, SOCE was significantly decreased upon istaroxime treatment. Furthermore, istaroxime strikingly diminished phosphorylated FAK levels. Interestingly, the efficacy of istaroxime on the inhibition of DU-145 cell migration was further enhanced by blocking Orai1 with 2-APB and FAK with the specific inhibitor PF-00562271. These results provide strong evidence that istaroxime prevents cell migration and motility of DU-145 prostate tumor cells, an effect at least partially attributed to Orai1 downregulation and FAK de-activation. CONCLUSION: Collectively our results indicate that this enzyme inhibitor, besides its pro-apoptotic action, affects motility of cancer cells, supporting its potential role as a strong candidate for further clinical cancer drug development.
[Mh] Termos MeSH primário: Movimento Celular/efeitos dos fármacos
Células Epiteliais/efeitos dos fármacos
Etiocolanolona/análogos & derivados
Quinase 1 de Adesão Focal/genética
Regulação Neoplásica da Expressão Gênica
Proteína ORAI1/genética
Bloqueadores dos Canais de Sódio/farmacologia
[Mh] Termos MeSH secundário: Cálcio/metabolismo
Canais de Cálcio/genética
Canais de Cálcio/metabolismo
Linhagem Celular Tumoral
Células Epiteliais/metabolismo
Células Epiteliais/patologia
Etiocolanolona/farmacologia
Corantes Fluorescentes/química
Quinase 1 de Adesão Focal/antagonistas & inibidores
Quinase 1 de Adesão Focal/metabolismo
Fura-2/química
Seres Humanos
Masculino
Proteínas de Neoplasias/antagonistas & inibidores
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Proteína ORAI1/antagonistas & inibidores
Proteína ORAI1/metabolismo
Fosforilação/efeitos dos fármacos
Próstata/efeitos dos fármacos
Próstata/metabolismo
Próstata/patologia
Inibidores de Proteínas Quinases/farmacologia
Pirimidinas/farmacologia
Transdução de Sinais
Molécula 1 de Interação Estromal/antagonistas & inibidores
Molécula 1 de Interação Estromal/genética
Molécula 1 de Interação Estromal/metabolismo
Sulfonamidas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels); 0 (Fluorescent Dyes); 0 (Neoplasm Proteins); 0 (ORAI1 Protein); 0 (ORAI1 protein, human); 0 (PF-00562271); 0 (Protein Kinase Inhibitors); 0 (Pyrimidines); 0 (STIM1 protein, human); 0 (Sodium Channel Blockers); 0 (Stromal Interaction Molecule 1); 0 (Sulfonamides); 97CGB1M48I (Etiocholanolone); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (PTK2 protein, human); SY7Q814VUP (Calcium); TSN3DL106G (Fura-2); W8I9H2TPPL (Istaroxime)
[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:170714
[St] Status:MEDLINE
[do] DOI:10.1159/000479200


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[PMID]:28687226
[Au] Autor:Cohen IS; Lin RZ; Ballou LM
[Ad] Endereço:Department of Physiology and Biophysics, The Institute for Molecular Cardiology, Stony Brook University, Stony Brook, NY. Electronic address: ira.cohen@stonybrook.edu.
[Ti] Título:Acquired long QT syndrome and phosphoinositide 3-kinase.
[So] Source:Trends Cardiovasc Med;27(7):451-459, 2017 Oct.
[Is] ISSN:1873-2615
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:While it is well known that mutation of several different ion channels can cause congenital long QT syndrome, block of I is widely thought to be responsible for most cases of drug-induced acquired long QT syndrome (aLQTS). In this article, we review evidence supporting another cause of aLQTS due to inhibition of phosphoinositide 3-kinase (PI3K) signaling. Inhibition of PI3K affects multiple plateau currents, reducing I , I , and I while increasing the persistent sodium current (I ). The effects of PI3K inhibitors develop slowly, requiring hours to days to reach steady state. Dofetilide and terfenadine, an antihistamine on which much of the original I hypothesis was based, are among the many drugs that inhibit the PI3K pathway. Reduced PI3K signaling may also play a role in aLQTS associated with diabetes. Drug safety testing to identify aLQTS risk may be improved by examining PI3K-dependent effects that develop over time.
[Mh] Termos MeSH primário: Sistema de Condução Cardíaco/efeitos dos fármacos
Frequência Cardíaca/efeitos dos fármacos
Síndrome do QT Longo/induzido quimicamente
Fosfatidilinositol 3-Quinase/antagonistas & inibidores
Inibidores de Proteínas Quinases/efeitos adversos
[Mh] Termos MeSH secundário: Potenciais de Ação
Animais
Sistema de Condução Cardíaco/enzimologia
Sistema de Condução Cardíaco/fisiopatologia
Seres Humanos
Síndrome do QT Longo/enzimologia
Síndrome do QT Longo/fisiopatologia
Fosfatidilinositol 3-Quinase/metabolismo
Bloqueadores dos Canais de Potássio/efeitos adversos
Fatores de Risco
Bloqueadores dos Canais de Sódio/efeitos adversos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Potassium Channel Blockers); 0 (Protein Kinase Inhibitors); 0 (Sodium Channel Blockers); EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170709
[St] Status:MEDLINE



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