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[PMID]:28391425
[Au] Autor:Anand S; Tong H; Besag FMC; Chan EW; Cortese S; Wong ICK
[Ad] Endereço:Department of Pharmacology and Pharmacy, Centre for Safe Medication Practice and Research, The University of Hong Kong, Pok Fu Lam, Hong Kong.
[Ti] Título:Safety, Tolerability and Efficacy of Drugs for Treating Behavioural Insomnia in Children with Attention-Deficit/Hyperactivity Disorder: A Systematic Review with Methodological Quality Assessment.
[So] Source:Paediatr Drugs;19(3):235-250, 2017 Jun.
[Is] ISSN:1179-2019
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: A large proportion of paediatric patients with attention-deficit/hyperactivity disorder (ADHD) have associated sleep problems which not only affect the child's wellbeing but also impact family functioning. Management of sleep problems is consequently an important aspect of overall ADHD management in paediatric patients. Although some drugs are being used off-label for the management of paediatric insomnia, there is scant clinical evidence supporting their use. Our aim was to identify and assess the quality of published studies reporting the safety, tolerability and efficacy of drugs used for treating behavioural insomnia in children with ADHD. METHODS: After an initial screen to determine which drugs were most commonly used, we conducted a systematic review of English-language publications from searches of PubMed, EMBASE, PsycINFO and two trial register databases to February 2017, using keywords 'clonidine', 'melatonin', 'zolpidem', 'eszopiclone', 'L-theanine', 'guanfacine', 'ADHD', 'sleep disorder' and 'children'. For quality assessment of included studies, we used the CONSORT checklist for randomised control trials (RCTs) and the Downs and Black checklist for non-RCTs. RESULTS: Twelve studies were included. Two case series for clonidine, two RCTs and four observational studies for melatonin and one RCT each for zolpidem, eszopiclone, L-theanine and guanfacine. Of the 12 included studies, only one on eszopiclone scored excellent for quality. The quality of the rest of the studies varied from moderate to low. For clonidine, melatonin and L-theanine, improvements in sleep-onset latency and total sleep duration were reported; however, zolpidem, eszopiclone and guanfacine failed to show any improvement when compared with placebo. Clonidine, melatonin, L-theanine, eszopiclone and guanfacine were well tolerated with mild to moderate adverse events; zolpidem was associated with neuropsychiatric adverse effects. CONCLUSION: There is generally poor evidence for prescribing drugs for behavioural insomnia in children with ADHD. Further controlled studies are warranted.
[Mh] Termos MeSH primário: Transtorno do Deficit de Atenção com Hiperatividade/tratamento farmacológico
Distúrbios do Início e da Manutenção do Sono/tratamento farmacológico
[Mh] Termos MeSH secundário: Transtorno do Deficit de Atenção com Hiperatividade/complicações
Transtorno do Deficit de Atenção com Hiperatividade/fisiopatologia
Criança
Clonidina/uso terapêutico
Zopiclona/uso terapêutico
Glutamatos/uso terapêutico
Guanfacina/uso terapêutico
Seres Humanos
Melatonina/uso terapêutico
Estudos Observacionais como Assunto
Piridinas/uso terapêutico
Ensaios Clínicos Controlados Aleatórios como Assunto
Distúrbios do Início e da Manutenção do Sono/complicações
Distúrbios do Início e da Manutenção do Sono/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Glutamates); 0 (Pyridines); 30OMY4G3MK (Guanfacine); 7K383OQI23 (zolpidem); 8021PR16QO (theanine); JL5DK93RCL (Melatonin); MN3L5RMN02 (Clonidine); UZX80K71OE (Eszopiclone)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170410
[St] Status:MEDLINE
[do] DOI:10.1007/s40272-017-0224-6


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[PMID]:28336568
[Au] Autor:Gratton C; Yousef S; Aarts E; Wallace DL; D'Esposito M; Silver MA
[Ad] Endereço:Neurology Department, Washington University, St. Louis, Missouri 63110, cgratton@wustl.edu.
[Ti] Título:Cholinergic, But Not Dopaminergic or Noradrenergic, Enhancement Sharpens Visual Spatial Perception in Humans.
[So] Source:J Neurosci;37(16):4405-4415, 2017 Apr 19.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The neuromodulator acetylcholine modulates spatial integration in visual cortex by altering the balance of inputs that generate neuronal receptive fields. These cholinergic effects may provide a neurobiological mechanism underlying the modulation of visual representations by visual spatial attention. However, the consequences of cholinergic enhancement on visuospatial perception in humans are unknown. We conducted two experiments to test whether enhancing cholinergic signaling selectively alters perceptual measures of visuospatial interactions in human subjects. In Experiment 1, a double-blind placebo-controlled pharmacology study, we measured how flanking distractors influenced detection of a small contrast decrement of a peripheral target, as a function of target-flanker distance. We found that cholinergic enhancement with the cholinesterase inhibitor donepezil improved target detection, and modeling suggested that this was mainly due to a narrowing of the extent of facilitatory perceptual spatial interactions. In Experiment 2, we tested whether these effects were selective to the cholinergic system or would also be observed following enhancements of related neuromodulators dopamine or norepinephrine. Unlike cholinergic enhancement, dopamine (bromocriptine) and norepinephrine (guanfacine) manipulations did not improve performance or systematically alter the spatial profile of perceptual interactions between targets and distractors. These findings reveal mechanisms by which cholinergic signaling influences visual spatial interactions in perception and improves processing of a visual target among distractors, effects that are notably similar to those of spatial selective attention. Acetylcholine influences how visual cortical neurons integrate signals across space, perhaps providing a neurobiological mechanism for the effects of visual selective attention. However, the influence of cholinergic enhancement on visuospatial perception remains unknown. Here we demonstrate that cholinergic enhancement improves detection of a target flanked by distractors, consistent with sharpened visuospatial perceptual representations. Furthermore, whereas most pharmacological studies focus on a single neurotransmitter, many neuromodulators can have related effects on cognition and perception. Thus, we also demonstrate that enhancing noradrenergic and dopaminergic systems does not systematically improve visuospatial perception or alter its tuning. Our results link visuospatial tuning effects of acetylcholine at the neuronal and perceptual levels and provide insights into the connection between cholinergic signaling and visual attention.
[Mh] Termos MeSH primário: Agonistas de Receptores Adrenérgicos alfa 2/farmacologia
Inibidores da Colinesterase/farmacologia
Sensibilidades de Contraste/efeitos dos fármacos
Agonistas de Dopamina/farmacologia
[Mh] Termos MeSH secundário: Adulto
Bromocriptina/farmacologia
Feminino
Guanfacina/farmacologia
Seres Humanos
Indanos/farmacologia
Masculino
Piperidinas/farmacologia
Distribuição Aleatória
Córtex Visual/efeitos dos fármacos
Córtex Visual/metabolismo
Córtex Visual/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Agonists); 0 (Cholinesterase Inhibitors); 0 (Dopamine Agonists); 0 (Indans); 0 (Piperidines); 30OMY4G3MK (Guanfacine); 3A64E3G5ZO (Bromocriptine); 8SSC91326P (donepezil)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171115
[Lr] Data última revisão:
171115
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2405-16.2017


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[PMID]:28063948
[Au] Autor:Turovsky EA; Turovskaya MV; Gaidin SG; Zinchenko VP
[Ad] Endereço:Institute of Cell Biophysics, Russian Academy of Sciences, Pushchino, Russia.
[Ti] Título:Cytokine IL-10, activators of PI3-kinase, agonists of α-2 adrenoreceptor and antioxidants prevent ischemia-induced cell death in rat hippocampal cultures.
[So] Source:Arch Biochem Biophys;615:35-43, 2017 Feb 01.
[Is] ISSN:1096-0384
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the present work we compared the protective effect of anti-inflammatory cytokine IL-10 with the action of a PI3-kinase selective activator 740 Y-P, selective agonists of alpha-2 adrenoreceptor, guanfacine and UK-14,304, and compounds having antioxidant effect: recombinant human peroxiredoxin 6 and B27, in hippocampal cell culture during OGD (ischemia-like conditions). It has been shown that the response of cells to OGD in the control includes two phases. The first phase was accompanied by an increase in the frequency of spontaneous synchronous Ca -oscillations (SSCO) in neurons and Ca -pulse in astrocytes. Spontaneous Ca events in astrocytes during ischemia in control experiments disappeared. The second phase started after a few minutes of OGD and looked like a sharp/avalanche, global synchronic (within 20 s) increase in [Ca ] in many cells. Within 1 h after OGD, a mass death of cells, primarily astrocytes, was observed. To study the protective action of the compounds, cells were incubated in the presence of the neuroprotective agents for 10-40 min or 24 h before ischemia. All the neuroprotective agents delayed a global [Ca ] increase during OGD or completely inhibited this process and increased cell survival.
[Mh] Termos MeSH primário: Antioxidantes/metabolismo
Hipocampo/citologia
Interleucina-10/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Receptores Adrenérgicos alfa 2/metabolismo
[Mh] Termos MeSH secundário: Agonistas Adrenérgicos/metabolismo
Animais
Astrócitos/citologia
Encéfalo/metabolismo
Cálcio/metabolismo
Morte Celular
Sobrevivência Celular
Células Cultivadas
Guanfacina/química
Isquemia/metabolismo
Oscilometria
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agonists); 0 (Antioxidants); 0 (Receptors, Adrenergic, alpha-2); 130068-27-8 (Interleukin-10); 30OMY4G3MK (Guanfacine); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170109
[St] Status:MEDLINE


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[PMID]:28001002
[Au] Autor:Duggins P; Stewart TC; Choo X; Eliasmith C
[Ad] Endereço:Centre for Theoretical Neuroscience, University of Waterloo.
[Ti] Título:The Effects of Guanfacine and Phenylephrine on a Spiking Neuron Model of Working Memory.
[So] Source:Top Cogn Sci;9(1):117-134, 2017 Jan.
[Is] ISSN:1756-8765
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We use a spiking neural network model of working memory (WM) capable of performing the spatial delayed response task (DRT) to investigate two drugs that affect WM: guanfacine (GFC) and phenylephrine (PHE). In this model, the loss of information over time results from changes in the spiking neural activity through recurrent connections. We reproduce the standard forgetting curve and then show that this curve changes in the presence of GFC and PHE, whose application is simulated by manipulating functional, neural, and biophysical properties of the model. In particular, applying GFC causes increased activity in neurons that are sensitive to the information currently being remembered, while applying PHE leads to decreased activity in these same neurons. Interestingly, these differential effects emerge from network-level interactions because GFC and PHE affect all neurons equally. We compare our model to both electrophysiological data from neurons in monkey dorsolateral prefrontal cortex and to behavioral evidence from monkeys performing the DRT.
[Mh] Termos MeSH primário: Guanfacina/farmacologia
Neurônios/efeitos dos fármacos
Fenilefrina/farmacologia
Córtex Pré-Frontal/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Haplorrinos
Seres Humanos
Memória de Curto Prazo/efeitos dos fármacos
Modelos Neurológicos
Neurônios/fisiologia
Córtex Pré-Frontal/fisiologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
1WS297W6MV (Phenylephrine); 30OMY4G3MK (Guanfacine)
[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:161222
[St] Status:MEDLINE
[do] DOI:10.1111/tops.12247


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[PMID]:28044946
[Au] Autor:Mattingly GW; Anderson RH
[Ad] Endereço:1Washington University School of Medicine,Department of Psychiatry and Behavioral Neurosciences,St. Charles,Missouri,USA.
[Ti] Título:Optimizing outcomes in ADHD treatment: from clinical targets to novel delivery systems.
[So] Source:CNS Spectr;21(S1):45-59, 2016 12.
[Is] ISSN:1092-8529
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Our knowledge and understanding of the underlying neurobiology and symptomatic expression of ADHD has advanced dramatically over the past decade. Associated with these advances has been a similar explosion of new treatment options to individualize treatment for our patients. This article will: ∙ review strategies to measure ADHD symptoms and functional difficulties while seeking to achieve full symptomatic remission throughout the day ∙ summarize recent findings regarding the management and prioritization of ADHD and comorbid conditions and ∙ discuss the various pharmacologic treatment options with a focus on recently developed molecules and novel delivery systems.
[Mh] Termos MeSH primário: Inibidores da Captação Adrenérgica/uso terapêutico
Agonistas de Receptores Adrenérgicos alfa 2/uso terapêutico
Transtorno do Deficit de Atenção com Hiperatividade/tratamento farmacológico
Estimulantes do Sistema Nervoso Central/administração & dosagem
[Mh] Termos MeSH secundário: Transtornos de Ansiedade/epidemiologia
Transtornos de Ansiedade/terapia
Cloridrato de Atomoxetina/uso terapêutico
Transtorno do Deficit de Atenção com Hiperatividade/epidemiologia
Transtorno Bipolar/epidemiologia
Transtorno Bipolar/terapia
Clonidina/uso terapêutico
Comorbidade
Preparações de Ação Retardada
Transtorno Depressivo/epidemiologia
Transtorno Depressivo/terapia
Dextroanfetamina/administração & dosagem
Guanfacina/uso terapêutico
Seres Humanos
Metilfenidato/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Adrenergic Uptake Inhibitors); 0 (Adrenergic alpha-2 Receptor Agonists); 0 (Central Nervous System Stimulants); 0 (Delayed-Action Preparations); 207ZZ9QZ49 (Methylphenidate); 30OMY4G3MK (Guanfacine); 57WVB6I2W0 (Atomoxetine Hydrochloride); MN3L5RMN02 (Clonidine); TZ47U051FI (Dextroamphetamine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170104
[St] Status:MEDLINE
[do] DOI:10.1017/S1092852916000808


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[PMID]:27828696
[Au] Autor:Jain R; Katic A
[Ad] Endereço:2500 W William Cannon Dr, Suite 505, Austin, TX 78745. JainTexas@gmail.com.
[Ti] Título:Current and Investigational Medication Delivery Systems for Treating Attention-Deficit/Hyperactivity Disorder.
[So] Source:Prim Care Companion CNS Disord;18(4), 2016 Aug 18.
[Is] ISSN:2155-7780
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To review currently available formulations and emphasize unmet needs in the pharmacologic management of attention-deficit/hyperactivity disorder (ADHD). DATA SOURCES: Publications and clinical trials were identified through PubMed and ClinicalTrials.gov, respectively. A Web-based search identified prescribing information for approved agents for treating ADHD, along with relevant guidelines and diagnostic criteria. STUDY SELECTION: The following search terms were used: (1) ADHD or attention-deficit/hyperactivity disorder or ADD or attention deficit hyperactivity disorder and/or (2) amphetamine or methylphenidate or atomoxetine or guanfacine or clonidine. Additional searches were performed using product brand names, and clinical trial was applied as a filter. Relevant studies were only included if published in English-language peer-reviewed journals and if involved agents were currently available (or pursuing approval) in the United States. Reviews of literature prior to 2005 and from 2005 to 2008 have been published previously; therefore, the present search focused on studies published from January 2009 through May 2016. In addition, reference lists of review articles and relevant studies were also examined to help identify additional studies. DATA EXTRACTION: A total of 578 publications were identified from the PubMed search, from which 426 publications were initially excluded based on review of the title and abstract. Reasons for exclusion included a focus on comorbid disorders, specific subpopulations, endpoints unrelated to improving ADHD symptomatology (eg, executive function, cognition, substance use), or quality of life measures. A more thorough assessment of the remaining citations, including publications and prescribing information, produced the final 219. RESULTS: Pharmacotherapy with stimulant and nonstimulant options is the most common approach for treating ADHD in adults and children. Stimulants are mostly formulated as either tablets or capsules; however, the newer generation includes transdermal patches, oral suspensions (liquids), chewable tablets, and orally disintegrating tablets. Nonstimulants are available in oral capsule (atomoxetine) and tablet (guanfacine and clonidine) formulations. CONCLUSIONS: Despite the broad range of treatment options currently available, nonadherence remains a significant problem in ADHD. While evidence is currently lacking, the availability of new formulations may improve adherence.
[Mh] Termos MeSH primário: Adrenérgicos/administração & dosagem
Adrenérgicos/uso terapêutico
Transtorno do Deficit de Atenção com Hiperatividade/tratamento farmacológico
Estimulantes do Sistema Nervoso Central/administração & dosagem
Estimulantes do Sistema Nervoso Central/uso terapêutico
[Mh] Termos MeSH secundário: Anfetaminas/administração & dosagem
Anfetaminas/uso terapêutico
Cloridrato de Atomoxetina/administração & dosagem
Cloridrato de Atomoxetina/uso terapêutico
Ensaios Clínicos como Assunto
Clonidina/administração & dosagem
Clonidina/uso terapêutico
Guanfacina/administração & dosagem
Guanfacina/uso terapêutico
Seres Humanos
Metilfenidato/administração & dosagem
Metilfenidato/uso terapêutico
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Amphetamines); 0 (Central Nervous System Stimulants); 207ZZ9QZ49 (Methylphenidate); 30OMY4G3MK (Guanfacine); 57WVB6I2W0 (Atomoxetine Hydrochloride); MN3L5RMN02 (Clonidine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170303
[Lr] Data última revisão:
170303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161110
[St] Status:MEDLINE
[do] DOI:10.4088/PCC.16r01979


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[PMID]:27669299
[Au] Autor:Klotz JL; Aiken GE; Bussard JR; Foote AP; Harmon DL; Goff BM; Schrick FN; Strickland JR
[Ad] Endereço:USDA-ARS, Forage-Animal Production Research Unit, Lexington, KY 40546, USA. james.klotz@ars.usda.gov.
[Ti] Título:Vasoactivity and Vasoconstriction Changes in Cattle Related to Time off Toxic Endophyte-Infected Tall Fescue.
[So] Source:Toxins (Basel);8(10), 2016 09 22.
[Is] ISSN:2072-6651
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Previous research has indicated that serotonergic and α-adrenergic receptors in peripheral vasculature are affected by exposure of cattle grazing toxic endophyte-infected (E+; Epichlöe coenophialia) tall fescue (Lolium arundinaceum). The objective of this experiment was to determine the period of time necessary for the vascular effects of ergot alkaloids to subside. Two experiments were conducted to investigate changes in vascular contractile response and vasoconstriction over time relative to removal from an ergot alkaloid-containing E+ tall fescue pasture. In Experiment 1, lateral saphenous vein biopsies were conducted on 21 predominantly Angus steers (357 ± 3 kg body weight) at 0 (n = 6), 7 (n = 6), 14 (n = 5), or 28 days (n = 4) after removal from grazing pasture (3.0 ha; endpoint ergovaline + ergovalinine = 1.35 mg/kg DM) for 126 days. In Experiment 2, lateral saphenous veins were biopsied from 24 Angus-cross steers (361 ± 4 kg body weight) at 0, 21, 42, and 63 days (n = 6 per time point) following removal from grazing tall fescue pastures (3.0 ha; first 88 days endpoint ergovaline + ergovalinine = 0.15 mg/kg DM; last 18 days endpoint ergovaline + ergovalinine = 0.57 mg/kg DM) for 106 total days. Six steers (370 ± 18 kg body weight) off of bermudagrass pasture for the same time interval were also biopsied on Day 0 and Day 63 (n = 3 per time point). Additionally, in Experiment 2, cross-sectional ultrasound scans of caudal artery at the fourth coccygeal vertebra were taken on Days 0, 8, 15, 21, 29, 36, 42, and 45 to determine mean artery luminal area to evaluate vasoconstriction. In both experiments, steers were removed from pasture and housed in a dry lot and fed a corn silage diet for the duration of biopsies and ultrasound scans. Biopsied vessels used to evaluate vasoactivity were cleaned, incubated in a multimyograph, and exposed to increasing concentrations of 4-Bromo-3,6-dimethoxybenzocyclobuten-1-yl) methylamine hydrobromide (TCB2; 5HT2A agonist), guanfacine (GF; α2A-adrenergic agonist), and (R)-(+)-m-nitrobiphenyline oxalate (NBP; α2C-adrenergic agonist) in both experiments and ergovaline (ERV) and ergotamine (ERT) in Experiments 1 and 2, respectively. In Experiment 1, days off pasture × agonist concentration was not significant (p > 0.1) for all four compounds tested. In Experiment 2, GF, NBP, TCB2 and ERT were significant for days off pasture × agonist concentration interaction (p < 0.02) and vasoactivity increased over time. Vasoactivity to agonists was reduced (p < 0.05) when steers were initially removed from E+ tall fescue pasture compared to bermudagrass, but did not differ by Day 63 for any variable. Luminal areas of caudal arteries in steers grazed on E+ tall fescue relaxed and were similar to steers that had grazed bermudagrass for 36 days on non-toxic diet (p = 0.15). These data demonstrate changes in peripheral vasoactivity and recovery from vasoconstriction occur beyond five weeks off toxic pasture and 5HT2A receptors appear to be more dramatically affected in the lateral saphenous vein by grazing E+ tall fescue pasture than adrenergic receptors.
[Mh] Termos MeSH primário: Endófitos/fisiologia
Epichloe/fisiologia
Festuca/microbiologia
Veia Safena/fisiologia
[Mh] Termos MeSH secundário: Agonistas de Receptores Adrenérgicos alfa 2/farmacologia
Animais
Compostos Bicíclicos com Pontes/farmacologia
Bovinos
Alcaloides de Claviceps/farmacologia
Comportamento Alimentar
Guanfacina/farmacologia
Masculino
Metilaminas/farmacologia
Prolactina/sangue
Veia Safena/efeitos dos fármacos
Agonistas de Receptores 5-HT2 de Serotonina/farmacologia
Vasoconstrição
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 ((4-bromo-3,6-dimethoxybenzocyclobuten-1-yl)methylamine); 0 (Adrenergic alpha-2 Receptor Agonists); 0 (Bridged Bicyclo Compounds); 0 (Ergot Alkaloids); 0 (Methylamines); 0 (Serotonin 5-HT2 Receptor Agonists); 30OMY4G3MK (Guanfacine); 9002-62-4 (Prolactin)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160927
[St] Status:MEDLINE


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[PMID]:27384184
[Au] Autor:Sansoè G; Aragno M; Mastrocola R; Mengozzi G; Parola M
[Ad] Endereço:Division of Gastroenterology, Gradenigo Hospital, Torino, Italy.
[Ti] Título:Alpha-2A Adrenoceptor Agonist Guanfacine Restores Diuretic Efficiency in Experimental Cirrhotic Ascites: Comparison with Clonidine.
[So] Source:PLoS One;11(7):e0158486, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In human cirrhosis, adrenergic hyperfunction causes proximal tubular fluid retention and contributes to diuretic-resistant ascites, and clonidine, a sympatholytic drug, improves natriuresis in difficult-to-treat ascites. AIM: To compare clonidine (aspecific α2-adrenoceptor agonist) to SSP-002021R (prodrug of guanfacine, specific α2A-receptor agonist), both associated with diuretics, in experimental cirrhotic ascites. METHODS AND RESULTS: Six groups of 12 rats were studied: controls (G1); controls receiving furosemide and potassium canrenoate (G2); rats with ascitic cirrhosis due to 14-week CCl4 treatment (G3); cirrhotic rats treated (over the 11th-14th CCl4 weeks) with furosemide and canrenoate (G4), furosemide, canrenoate and clonidine (G5), or diuretics and SSP002021R (G6). Three rats of each group had their hormonal status and renal function assessed at the end of 11th, 12th, 13th, and 14th weeks of respective treatments.Cirrhotic rats in G3 and G4 gained weight over the 12th-14th CCl4 weeks. In G4, brief increase in sodium excretion over the 11th-12th weeks preceded worsening of inulin clearance and natriuresis (diuretic resistance). In comparison with G4, the addition of clonidine (G5) or guanfacine (G6) to diuretics improved, respectively, sodium excretion over the 11th-12th CCl4 weeks, or GFR and electrolytes excretion over the 13th-14th CCl4 weeks. Natriuretic responses in G5 and G6 were accompanied by reduced catecholamine serum levels. CONCLUSIONS: α2A-receptor agonists restore glomerular filtration rate and natriuresis, and delay diuretic-resistant ascites in experimental advanced cirrhosis. Clonidine ameliorates diuretic-dependent natriuresis just for a short time.
[Mh] Termos MeSH primário: Agonistas Adrenérgicos/uso terapêutico
Ascite/tratamento farmacológico
Clonidina/uso terapêutico
Diuréticos/uso terapêutico
Fibrose/tratamento farmacológico
Guanfacina/análogos & derivados
Guanfacina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Ácido Canrenoico/administração & dosagem
Clonidina/administração & dosagem
Sinergismo Farmacológico
Furosemida/administração & dosagem
Guanfacina/química
Masculino
Ratos
Ratos Wistar
Receptores Adrenérgicos alfa 2/química
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agonists); 0 (Diuretics); 0 (Receptors, Adrenergic, alpha-2); 30OMY4G3MK (Guanfacine); 7LXU5N7ZO5 (Furosemide); 87UG89VA9K (Canrenoic Acid); MN3L5RMN02 (Clonidine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160708
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0158486


  9 / 631 MEDLINE  
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[PMID]:27254403
[Au] Autor:Alamo C; López-Muñoz F; Sánchez-García J
[Ad] Endereço:Department of Biomedical Sciences. School of Medicine and Health Sciences. University of Alcalá
[Ti] Título:Mechanism of action of guanfacine: a postsynaptic differential approach to the treatment of attention deficit hyperactivity disorder (adhd).
[So] Source:Actas Esp Psiquiatr;44(3):107-12, 2016 May.
[Is] ISSN:1578-2735
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:The treatment of ADHD has focused on the use of psychostimulants drugs such as methylphenidate or amphetamine and derivatives, or not stimulants agents, such as atomoxetine. These agents act mainly on catecholaminergic presynaptic mechanisms. Recently the European Medicines Agency (EMA) has approved another not psychostimulant drug, guanfacine extended release (ER), as a new option to the treatment of ADHD, which acts at postsynaptic level. Guanfacine stimulates postsynaptic alfa-2A adrenergic receptors so it inhibits the production of cAMP and closes HCN channels enhancing the effectiveness of the signal of the pyramidal neurons of the prefrontal cortex (PFC), thus improving working memory and attention. In addition, stimulation of the alpha-2A receptors promotes growth and maturation of the dendritic spines of pyramidal neurons of the medial PFc, that are associated with brain function such as learning and memory. In contrast with psychostimulants or atomoxetine, guanfacine mimics noradrenaline stimulation of postsynaptic receptors alfa-2A on the PFC.
[Mh] Termos MeSH primário: Agonistas de Receptores Adrenérgicos alfa 2/farmacologia
Agonistas de Receptores Adrenérgicos alfa 2/uso terapêutico
Transtorno do Deficit de Atenção com Hiperatividade/tratamento farmacológico
Guanfacina/farmacologia
Guanfacina/uso terapêutico
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Agonists); 30OMY4G3MK (Guanfacine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160603
[St] Status:MEDLINE


  10 / 631 MEDLINE  
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[PMID]:27236168
[Au] Autor:Mattes JA
[Ad] Endereço:Dr. Mattes is Director, Psychopharmacology Research Association, Princeton, NJ. jmattesmd@verizon.net.
[Ti] Título:Treating ADHD in Prison: Focus on Alpha-2 Agonists (Clonidine and Guanfacine).
[So] Source:J Am Acad Psychiatry Law;44(2):151-7, 2016 Jun.
[Is] ISSN:1943-3662
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Attention deficit/hyperactivity disorder (ADHD) is prevalent in prison populations, but optimal treatment recommendations in prison are uncertain. Stimulants are problematic because of the potential for abuse. This article is a review of medication options for ADHD, focusing on the α2 agonists clonidine and guanfacine, which, in their extended-release (ER) forms, are U.S. Food and Drug Administration (FDA) approved for the treatment of ADHD, although they are probably less efficacious, overall, than stimulants. Advantages of α2 agonists in prison include: they are not controlled substances and have no known abuse potential; they may be particularly helpful for ADHD with associated aggression and other features of conduct disorder; they may reduce anxiety and symptoms of posttraumatic stress disorder; and they are somewhat sedating. The pharmacology of these agents and the presumed mechanism of action are discussed, including the fact that guanfacine more specifically affects α2A receptors, which are postsynaptic in the frontal cortex. Other differences between clonidine and guanfacine and between the generic immediate-release (IR) forms and the ER forms are also discussed. The IR forms, while themselves not FDA approved for ADHD, may, with dosage adjustment, be reasonable alternatives (with considerable cost savings). Overall, given the FDA-accepted evidence of efficacy, the lack of abuse potential, and the favorable side effect profile, α agonists may be the treatment of choice for prison inmates with ADHD.
[Mh] Termos MeSH primário: Agonistas de Receptores Adrenérgicos alfa 2/uso terapêutico
Transtorno do Deficit de Atenção com Hiperatividade/tratamento farmacológico
Clonidina/uso terapêutico
Guanfacina/uso terapêutico
Prisioneiros/psicologia
[Mh] Termos MeSH secundário: Seres Humanos
Estados Unidos
United States Food and Drug Administration
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Agonists); 30OMY4G3MK (Guanfacine); MN3L5RMN02 (Clonidine)
[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:160529
[St] Status:MEDLINE



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