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[PMID]:28482223
[Au] Autor:Peng W; Ding F; Peng YK; Xie Y
[Ad] Endereço:College of Plant Protection, Qingdao Agricultural University, Qingdao 266109, China; College of Food Science and Engineering, Qingdao Agricultural University, Qingdao 266109, China; Department of Chemistry, China Agricultural University, Beijing 100193, China.
[Ti] Título:Biological effects of α-adrenergic phentolamine on erythrocyte hemeprotein: Molecular insights from biorecognition behavior, protein dynamics and flexibility.
[So] Source:J Photochem Photobiol B;171:75-84, 2017 Jun.
[Is] ISSN:1873-2682
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Phentolamine is one of the most representative nonselective α-adrenoreceptor blocking agents, which have been proved to be owned various pharmacological actions. Unfortunately, whether erythrocytes in the veins intervene in biological behaviors of such drug are largely obscured. With the aid of multiple biophysical techniques, this scenario was to detailed explore the potential biorecognition between phentolamine and the hemeprotein in the cytosol of erythrocytes, and the influences of dynamic characters of protein during the bioreaction. Steady-state and time-resolved fluorescence data manifested that the biomolecular recognition of phentolamine by hemeprotein was processed through the biopolymer-drug adduct with a moderate strength of 10 M . Such procedure causes a reduction in fluorescence intensity of the aromatic tryptophan (Trp) residues, and the R-T transition of the globular protein occurred concurrently. Circular dichroism demonstrated the conclusions of fluorescence essays, viz. biorecognition can induce fairly structural transformation (self-regulation) of protein conformation. Furthermore, one could find that a specific domain for phentolamine is located at the polypeptide chains α ß interface, and hydrogen bonds, π-conjugated and hydrophobic effects are discovered to be held the lowest energy state of the biomacromolecule-drug biosystem, which overtly matches the outcomes of wet experiments. Meanwhile, several crucial residues such as Trp-37 and Arg-40 were confirmed to have directly noncovalent interactions with phentolamine, and the effect of the heme group on the biomolecule-drug recognition is minimal. Further analyses of molecular dynamics simulation supported that the inherent protein flexibility may notably elicit alterations in some key noncovalent bonds between biomacromolecule and drug during the dynamic biointeraction, which might primarily be attributed to the torsion of drug structure and the conformational changes of essential residues. Undoubtedly, this research will not only help to thoroughly unearth the pharmacological profiles of phentolamine, but to elaborate the impacts of the intrinsic features (i.e. dynamics and flexibility) of critically cellular proteins on the biological conducts of active α-adrenergic blockers.
[Mh] Termos MeSH primário: Hemeproteínas/metabolismo
Fentolamina/toxicidade
[Mh] Termos MeSH secundário: Sítios de Ligação
Dicroísmo Circular
Eritrócitos/citologia
Eritrócitos/efeitos dos fármacos
Eritrócitos/metabolismo
Hemeproteínas/química
Seres Humanos
Ligações de Hidrogênio
Interações Hidrofóbicas e Hidrofílicas
Simulação de Acoplamento Molecular
Simulação de Dinâmica Molecular
Estrutura Terciária de Proteína
Espectrometria de Fluorescência
Triptofano/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hemeproteins); 8DUH1N11BX (Tryptophan); Z468598HBV (Phentolamine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170509
[St] Status:MEDLINE


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[PMID]:28202248
[Au] Autor:Okada S; Yamaguchi N
[Ad] Endereço:Department of Pharmacology, Graduate School of Medicine, Aichi Medical University, 1-1 Yazakokarimata, Nagakute, Aichi 480-1195, Japan. Electronic address: okadas@aichi-med-u.ac.jp.
[Ti] Título:Possible role of adrenoceptors in the hypothalamic paraventricular nucleus in corticotropin-releasing factor-induced sympatho-adrenomedullary outflow in rats.
[So] Source:Auton Neurosci;203:74-80, 2017 Mar.
[Is] ISSN:1872-7484
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: A functional interaction between the corticotropin-releasing factor (CRF) system and noradrenergic neurons in the brain has been suggested. In the present study, we investigated the interrelationship between the central CRF-induced elevation of plasma catecholamines and adrenoceptor activation in the paraventricular nucleus of the hypothalamus (PVN) using urethane-anesthetized rats. MAIN METHODS: In rats under urethane anesthesia, a femoral venous line was inserted for infusion of saline, and a femoral arterial line was inserted for collecting blood samples. Next, animals were placed in a stereotaxic apparatus for the application of test agents. Catecholamines in the plasma were extracted by alumina absorption and were assayed with high-performance liquid chromatography with electrochemical detection. Quantification of noradrenaline in rat PVN microdialysates was performed with high-performance liquid chromatography with electrochemical detection. KEY FINDINGS: We showed that centrally administered CRF elevated noradrenaline release in the PVN. Furthermore, we demonstrated that microinjection of phenylephrine into the PVN induced elevation of plasma levels of adrenaline, but not of noradrenaline, whereas microinjection of isoproterenol into the PVN induced elevation of plasma levels of noradrenaline, but not of adrenaline. Bilateral blockade of adrenoceptors in the PVN revealed that phentolamine significantly suppressed the CRF-induced elevation of plasma adrenaline level, while propranolol significantly CRF-induced elevation of plasma noradrenaline level. SIGNIFICANCE: Our results suggest that centrally administered CRF-induced elevation of plasma levels of adrenaline and noradrenaline can be mediated via activation of α-adrenoceptors and ß-adrenoceptors, respectively, in the rat PVN.
[Mh] Termos MeSH primário: Medula Suprarrenal/efeitos dos fármacos
Hormônio Liberador da Corticotropina/administração & dosagem
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Receptores Adrenérgicos alfa/metabolismo
Receptores Adrenérgicos beta/metabolismo
Sistema Nervoso Simpático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Medula Suprarrenal/metabolismo
Adrenérgicos/farmacologia
Anestésicos Intravenosos/farmacologia
Animais
Hormônio Liberador da Corticotropina/metabolismo
Epinefrina/sangue
Isoproterenol/farmacologia
Masculino
Norepinefrina/sangue
Núcleo Hipotalâmico Paraventricular/metabolismo
Fentolamina/farmacologia
Fenilefrina/farmacologia
Propranolol/farmacologia
Ratos Wistar
Sistema Nervoso Simpático/metabolismo
Simpatomiméticos/farmacologia
Uretana/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agents); 0 (Anesthetics, Intravenous); 0 (Receptors, Adrenergic, alpha); 0 (Receptors, Adrenergic, beta); 0 (Sympathomimetics); 1WS297W6MV (Phenylephrine); 3IN71E75Z5 (Urethane); 9015-71-8 (Corticotropin-Releasing Hormone); 9Y8NXQ24VQ (Propranolol); L628TT009W (Isoproterenol); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine); Z468598HBV (Phentolamine)
[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:170217
[St] Status:MEDLINE


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[PMID]:28115396
[Au] Autor:Morton GJ; Muta K; Kaiyala KJ; Rojas JM; Scarlett JM; Matsen ME; Nelson JT; Acharya NK; Piccinini F; Stefanovski D; Bergman RN; Taborsky GJ; Kahn SE; Schwartz MW
[Ad] Endereço:University of Washington Diabetes Institute, Department of Medicine, University of Washington, Seattle, WA.
[Ti] Título:Evidence That the Sympathetic Nervous System Elicits Rapid, Coordinated, and Reciprocal Adjustments of Insulin Secretion and Insulin Sensitivity During Cold Exposure.
[So] Source:Diabetes;66(4):823-834, 2017 Apr.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dynamic adjustment of insulin secretion to compensate for changes of insulin sensitivity that result from alteration of nutritional or metabolic status is a fundamental aspect of glucose homeostasis. To investigate the role of the brain in this coupling process, we used cold exposure as an experimental paradigm because the sympathetic nervous system (SNS) helps to coordinate the major shifts of tissue glucose utilization needed to ensure that increased thermogenic needs are met. We found that glucose-induced insulin secretion declined by 50% in rats housed at 5°C for 28 h, and yet, glucose tolerance did not change, owing to a doubling of insulin sensitivity. These potent effects on insulin secretion and sensitivity were fully reversed by returning animals to room temperature (22°C) for 4 h or by intravenous infusion of the α-adrenergic receptor antagonist phentolamine for only 30 min. By comparison, insulin clearance was not affected by cold exposure or phentolamine infusion. These findings offer direct evidence of a key role for the brain, acting via the SNS, in the rapid, highly coordinated, and reciprocal changes of insulin secretion and insulin sensitivity that preserve glucose homeostasis in the setting of cold exposure.
[Mh] Termos MeSH primário: Glicemia/metabolismo
Temperatura Baixa
Resistência à Insulina
Insulina/secreção
Sistema Nervoso Simpático/metabolismo
[Mh] Termos MeSH secundário: Antagonistas Adrenérgicos alfa/farmacologia
Animais
Glicemia/efeitos dos fármacos
Técnica Clamp de Glucose
Insulina/metabolismo
Masculino
Fentolamina/farmacologia
Ratos
Ratos Long-Evans
Ratos Wistar
Sistema Nervoso Simpático/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-Antagonists); 0 (Blood Glucose); 0 (Insulin); Z468598HBV (Phentolamine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170125
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1351


  4 / 8691 MEDLINE  
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[PMID]:27314442
[Au] Autor:Pan L; Liu C; Kong Y; Piao Z; Cheng B
[Ad] Endereço:Southern Medical University, Guangzhou, China.
[Ti] Título:Phentolamine inhibits angiogenesis in vitro: Suppression of proliferation migration and differentiation of human endothelial cells.
[So] Source:Clin Hemorheol Microcirc;65(1):31-41, 2017.
[Is] ISSN:1875-8622
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:It is widely known that the ß-adrenergic receptor (AR) blocker (propranolol) inhibits human endothelial cell (EC) angiogenesis in vitro, but how the α-AR antagonist (phentolamine) affects human EC angiogenesis has not yet been studied. Here, we show for the first time that both human dermal microvascular ECs (HDMECs) and human brain microvascular ECs (HBMECs) express α-ARs. Moreover, our results indicate that phentolamine inhibits the proliferation, migration, and tubulogenesis of HDMECs and HBMECs. Finally, VEGFR-2 and Ang1/2 expression of HDMECs was suppressed by phentolamine. Together, these results indicate that phentolamine impairs several critical events of neovascularization, and α-ARs, as well as the VEGF/VEGFR-2 and Ang/Tie-2 signaling pathways, may be involved in these processes. Our results suggest a novel therapeutic strategy for the use of α-blockers in the treatment of human angiogenesis-dependent diseases.
[Mh] Termos MeSH primário: Antagonistas Adrenérgicos alfa/uso terapêutico
Células Endoteliais/efeitos dos fármacos
Fentolamina/uso terapêutico
[Mh] Termos MeSH secundário: Antagonistas Adrenérgicos alfa/administração & dosagem
Animais
Diferenciação Celular
Movimento Celular
Proliferação Celular
Células Endoteliais/citologia
Células Endoteliais/metabolismo
Seres Humanos
Neovascularização Patológica/metabolismo
Fentolamina/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-Antagonists); Z468598HBV (Phentolamine)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170426
[Lr] Data última revisão:
170426
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160618
[St] Status:MEDLINE
[do] DOI:10.3233/CH-162070


  5 / 8691 MEDLINE  
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[PMID]:28965383
[Au] Autor:Wang GY; Xu CC; Wu KR; Liu GL; Zhang J; Pan YN; Tang YF
[Ad] Endereço:Department of Urology, Ningbo First Hospital, Ningbo, Zhejiang, 315010, China.
[Ti] Título:[Application value of Toshiba 320-row dynamic volumetric CT angiography in the diagnosis of venous erectile dysfunction].
[So] Source:Zhonghua Nan Ke Xue;22(7):635-640, 2016 07.
[Is] ISSN:1009-3591
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Objective: To investigate the application value of Toshiba 320-row dynamic volumetric CT angiography in the diagnosis of venous erectile dysfunction (VED). METHODS: We enrolled in this study 33 patients diagnosed with ED by audiovisual sexual stimulation screening in the outpatient department. Penile erection was induced in the patients by injection of 2 mg phentolamine plus 30 mg papaverine into the corpus cavernosum, followed by that of contrast agent of iobitridol through the vein and corpus cavernosum successively. Then 320-row dynamic volumetric CT angiography was performed and the images of the corpus cavernosum in the arterial and venous phases were collected and processed. RESULTS: Different degrees of abnormal venous drainage were observed in 29 of the patients, including 7 cases (24.1%) of back deep venous leakage, 6 cases (20.7%) of foot venous leakage, 3 cases (10.3%) of dorsal superficial venous leakage, 1 case (3.5%) of intervertebral venous leakage, 2 cases (6.9%) of cavernous venous leakage, and 10 cases (34.5%) of mixed venous leakage. Ten of the patients underwent surgery, dorsal deep penile vein ligation in 2 cases, dorsal deep vein embedding plus foot vein ligation in 4, and foot vein ligation in the other 4. Eight of the patients were followed up for 3-12 months post-operatively, during which 2 achieved obvious erectile improvement, while the other 6 gained normal penile erection. CONCLUSIONS: Toshiba 320-row dynamic volumetric CT angiography is a reliable method for the diagnosis of VED, which displays the precise location of venous leakage for clinical treatment, with the advantages of clearer images, lower doses of contrast agent and radiation, and faster examination than X-ray penile angiography.
[Mh] Termos MeSH primário: Angiografia por Tomografia Computadorizada
Disfunção Erétil/diagnóstico por imagem
[Mh] Termos MeSH secundário: Adulto
Artérias/diagnóstico por imagem
Meios de Contraste
Combinação de Medicamentos
Seres Humanos
Injeções
Iohexol/análogos & derivados
Ligadura
Masculino
Meia-Idade
Papaverina/administração & dosagem
Ereção Peniana
Pênis/diagnóstico por imagem
Pênis/fisiopatologia
Fentolamina/administração & dosagem
Veias/diagnóstico por imagem
Veias/cirurgia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Contrast Media); 0 (Drug Combinations); 0 (papaverine, phentolamine drug combination); 182ECH14UH (iobitridol); 4419T9MX03 (Iohexol); DAA13NKG2Q (Papaverine); Z468598HBV (Phentolamine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171002
[St] Status:MEDLINE


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[PMID]:27421789
[Au] Autor:Aydin TH; Can ÖD; Demir Özkay Ü; Turan N
[Ad] Endereço:Department of Pharmacology, Faculty of Pharmacy, Anadolu University, 26470, Eskisehir, Turkey.
[Ti] Título:Effect of subacute agomelatine treatment on painful diabetic neuropathy: involvement of catecholaminergic mechanisms.
[So] Source:Fundam Clin Pharmacol;30(6):549-567, 2016 Dec.
[Is] ISSN:1472-8206
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In this study, we investigated the effects of subacute agomelatine (40 and 80 mg/kg) administration on chronic hyperglycemia, metabolic parameters, and pain perception in streptozotocin-induced diabetic rats. Fasting blood glucose measurements and oral glucose tolerance tests were performed to evaluate the effect of agomelatine on glycemia, while metabolic parameters were monitored using metabolic cages. Potential effect of agomelatine on diabetes-induced mechanical and thermal allodynia was evaluated using dynamic plantar aesthesiometer and warm plate (38 °C) tests, respectively. Additionally, influence of agomelatine on hyperalgesia occurring in connection with diabetic neuropathy was examined using the Randall-Selitto (mechanical nociceptive stimulus), Hargreaves (thermal nociceptive stimulus), and cold plate (4 °C, thermal nociceptive stimulus) tests. Obtained data indicated that, in diabetic rats, agomelatine significantly improved hyperalgesia and allodynia responses, without no effect on hyperglycemia or the associated polydipsia, polyuria, and hyperphagia. Therapeutic potential of agomelatine on neuropathic pain was suppressed with α-methyl-para-tyrosine methyl ester (an inhibitor of catecholamine synthesis), phentolamine (a nonselective α-adrenoceptor antagonist), and propranolol (a nonselective ß-adrenoceptor antagonist) administrations. However, p-chlorophenylalanine methyl ester (an inhibitor of serotonin synthesis) pretreatment could not be achieved to reverse these antihyperalgesic and antiallodynic effects. These results suggest that the curative effect of agomelatine on neuropathic pain is mediated through rising synaptic catecholamine levels as well as through interactions with both α- and ß-adrenoceptors. To our knowledge, this is the first study to show findings that indicate catecholaminergic system mediated antihyperalgesic and antiallodynic effects of agomelatine.
[Mh] Termos MeSH primário: Acetamidas/farmacologia
Catecolaminas/metabolismo
Neuropatias Diabéticas/tratamento farmacológico
Neuralgia/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Glicemia/efeitos dos fármacos
Diabetes Mellitus Experimental/induzido quimicamente
Diabetes Mellitus Experimental/complicações
Diabetes Mellitus Experimental/metabolismo
Neuropatias Diabéticas/etiologia
Neuropatias Diabéticas/metabolismo
Fenclonina/análogos & derivados
Fenclonina/farmacologia
Hiperalgesia/tratamento farmacológico
Hiperalgesia/metabolismo
Hiperglicemia/tratamento farmacológico
Hiperglicemia/metabolismo
Metiltirosinas/farmacologia
Neuralgia/metabolismo
Fentolamina/farmacologia
Propranolol/farmacologia
Ratos
Ratos Sprague-Dawley
Receptores Adrenérgicos alfa/metabolismo
Receptores Adrenérgicos beta/metabolismo
Estreptozocina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Acetamides); 0 (Blood Glucose); 0 (Catecholamines); 0 (Methyltyrosines); 0 (Receptors, Adrenergic, alpha); 0 (Receptors, Adrenergic, beta); 138112-76-2 (S 20098); 23434-96-0 (4-chlorophenylalanine methyl ester); 4502-13-0 (alpha-methyltyrosine methyl ester); 5W494URQ81 (Streptozocin); 9Y8NXQ24VQ (Propranolol); R5J7E3L9SP (Fenclonine); Z468598HBV (Phentolamine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170328
[Lr] Data última revisão:
170328
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160717
[St] Status:MEDLINE
[do] DOI:10.1111/fcp.12224


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[PMID]:27367668
[Au] Autor:Bragiel AM; Wang D; Pieczonka TD; Shono M; Ishikawa Y
[Ad] Endereço:Department of Medical Pharmacology, Institute of Biomedical Sciences, Tokushima University Graduate School, 3-18-15, Kuramoto-cho, Tokushima 770-8504, Japan. aneta.bragiel@gmail.com.
[Ti] Título:Mechanisms Underlying Activation of α1-Adrenergic Receptor-Induced Trafficking of AQP5 in Rat Parotid Acinar Cells under Isotonic or Hypotonic Conditions.
[So] Source:Int J Mol Sci;17(7), 2016 Jun 28.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Defective cellular trafficking of aquaporin-5 (AQP5) to the apical plasma membrane (APM) in salivary glands is associated with the loss of salivary fluid secretion. To examine mechanisms of α1-adrenoceptor (AR)-induced trafficking of AQP5, immunoconfocal microscopy and Western blot analysis were used to analyze AQP5 localization in parotid tissues stimulated with phenylephrine under different osmolality. Phenylephrine-induced trafficking of AQP5 to the APM and lateral plasma membrane (LPM) was mediated via the α1A-AR subtype, but not the α1B- and α1D-AR subtypes. Phenylephrine-induced trafficking of AQP5 was inhibited by ODQ and KT5823, inhibitors of nitric oxide (NO)-stimulated guanylcyclase (GC) and protein kinase (PK) G, respectively, indicating the involvement of the NO/ soluble (c) GC/PKG signaling pathway. Under isotonic conditions, phenylephrine-induced trafficking was inhibited by La(3+), implying the participation of store-operated Ca(2+) channel. Under hypotonic conditions, phenylephrine-induced trafficking of AQP5 to the APM was higher than that under isotonic conditions. Under non-stimulated conditions, hypotonicity-induced trafficking of AQP5 to the APM was inhibited by ruthenium red and La(3+), suggesting the involvement of extracellular Ca(2+) entry. Thus, α1A-AR activation induced the trafficking of AQP5 to the APM and LPM via the Ca(2+)/ cyclic guanosine monophosphate (cGMP)/PKG signaling pathway, which is associated with store-operated Ca(2+) entry.
[Mh] Termos MeSH primário: Células Acinares/metabolismo
Aquaporina 5/metabolismo
Glândula Parótida/citologia
Receptores Adrenérgicos alfa 1/metabolismo
[Mh] Termos MeSH secundário: Células Acinares/efeitos dos fármacos
Agonistas de Receptores Adrenérgicos alfa 1/farmacologia
Antagonistas de Receptores Adrenérgicos alfa 1/farmacologia
Animais
Membrana Celular/efeitos dos fármacos
Membrana Celular/metabolismo
Gangliosídeo G(M1)/metabolismo
Soluções Hipotônicas/farmacologia
Imuno-Histoquímica
Soluções Isotônicas/farmacologia
Masculino
Fentolamina/farmacologia
Fenilefrina/farmacologia
Transporte Proteico/efeitos dos fármacos
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-1 Receptor Agonists); 0 (Adrenergic alpha-1 Receptor Antagonists); 0 (Aquaporin 5); 0 (Hypotonic Solutions); 0 (Isotonic Solutions); 0 (Receptors, Adrenergic, alpha-1); 1WS297W6MV (Phenylephrine); 37758-47-7 (G(M1) Ganglioside); Z468598HBV (Phentolamine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170321
[Lr] Data última revisão:
170321
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160702
[St] Status:MEDLINE


  8 / 8691 MEDLINE  
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[PMID]:27317352
[Au] Autor:Zhang S; Johnson CM; Cui N; Xing H; Zhong W; Wu Y; Jiang C
[Ad] Endereço:Department of Biology, Georgia State University, 100 Piedmont Avenue, Atlanta, GA 30302.
[Ti] Título:An optogenetic mouse model of rett syndrome targeting on catecholaminergic neurons.
[So] Source:J Neurosci Res;94(10):896-906, 2016 Oct.
[Is] ISSN:1097-4547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rett syndrome (RTT) is a neurodevelopmental disorder affecting multiple functions, including the norepinephrine (NE) system. In the CNS, NE is produced mostly by neurons in the locus coeruleus (LC), where defects in intrinsic neuronal properties, NE biosynthetic enzymes, neuronal CO2 sensitivity, and synaptic currents have been reported in mouse models of RTT. LC neurons in methyl-CpG-binding protein 2 gene (Mecp2) null mice show a high rate of spontaneous firing, although whether such hyperexcitability might increase or decrease the NE release from synapses is unknown. To activate the NEergic axonal terminals selectively, we generated an optogenetic mouse model of RTT in which NEergic neuronal excitability can be manipulated with light. Using commercially available mouse breeders, we produced a new strain of double-transgenic mice with Mecp2 knockout and channelrhodopsin (ChR) knockin in catecholaminergic neurons. Several RTT-like phenotypes were found in the tyrosine hydroxylase (TH)-ChR-Mecp2(-/Y) mice, including hypoactivity, low body weight, hindlimb clasping, and breathing disorders. In brain slices, optostimulation produced depolarization and an increase in the firing rate of LC neurons from TH-ChR control mice. In TH-ChR control mice, optostimulation of presynaptic NEergic neurons augmented the firing rate of hypoglossal neurons (HNs), which was blocked by the α-adrenoceptor antagonist phentolamine. Such optostimulation of NEergic terminals had almost no effect on HNs from two or three TH-ChR-Mecp2(-/Y) mice, indicating that excessive excitation of presynaptic neurons does not benefit NEergic modulation in mice with Mecp2 disruption. These results also demonstrate the feasibility of generating double-transgenic mice for studies of RTT with commercially available mice, which are inexpensive, labor/time efficient, and promising for cell-specific stimulation. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Modelos Animais de Doenças
Locus Cerúleo/patologia
Neurônios/fisiologia
Norepinefrina/metabolismo
Optogenética
Síndrome de Rett/genética
Síndrome de Rett/patologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Potenciais de Ação/genética
Antagonistas Adrenérgicos alfa/farmacologia
Animais
Dopamina beta-Hidroxilase/metabolismo
Feminino
Proteínas Luminescentes/genética
Proteínas Luminescentes/metabolismo
Masculino
Proteína 2 de Ligação a Metil-CpG/genética
Proteína 2 de Ligação a Metil-CpG/metabolismo
Camundongos
Camundongos Transgênicos
Neurônios/efeitos dos fármacos
Fentolamina/farmacologia
Síndrome de Rett/fisiopatologia
Rodopsina/genética
Rodopsina/metabolismo
Tirosina 3-Mono-Oxigenase/genética
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-Antagonists); 0 (Luminescent Proteins); 0 (Methyl-CpG-Binding Protein 2); 9009-81-8 (Rhodopsin); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); EC 1.14.17.1 (Dopamine beta-Hydroxylase); X4W3ENH1CV (Norepinephrine); Z468598HBV (Phentolamine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160619
[St] Status:MEDLINE
[do] DOI:10.1002/jnr.23760


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[PMID]:27187577
[Au] Autor:Matsuo R; Tanaka M; Fukata R; Kobayashi S; Aonuma H; Matsuo Y
[Ad] Endereço:International College of Arts and Sciences, Fukuoka Women's University, Higashi-ku, Fukuoka, 813-8529, Japan. matsuor@fwu.ac.jp.
[Ti] Título:Octopaminergic system in the central nervous system of the terrestrial slug Limax.
[So] Source:J Comp Neurol;524(18):3849-3864, 2016 Dec 15.
[Is] ISSN:1096-9861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The terrestrial slug Limax can learn to avoid the odor of some food (e.g., carrot juice) by the simultaneous presentation of an aversive stimulus (e.g., bitterness of quinidine). This type of associative memory critically depends on the higher olfactory center, the procerebrum in the central nervous system. The modulation of the local field potential (LFP) oscillation recorded on the procerebrum has been thought to reflect the information processing of the odor that elicits the behavioral change, such as avoidance of the aversively learned odor or approaching an attractive food's odor. Here we focused on octopamine, an important neuromodulator involved in learning and memory in invertebrates, and considered to be the invertebrate equivalent of noradrenaline. We identified a few octopaminergic neurons in the subesophageal and buccal ganglia, and a larger number near the procerebrum in the cerebral ganglia, using immunohistochmical staining and in situ hybridization of tyramine ß-hydroxylase, an octopamine-synthesizing enzyme. Application of octopamine reduced the frequency of LFP oscillation in a dose-dependent manner, and this effect was inhibited by preincubation with phentolamine. High-performance liquid chromatography analysis revealed the presence of octopamine, noradrenaline, and adrenaline in the central nervous system. Unexpectedly, noradrenaline and adrenaline both accelerated the LFP oscillation, in contrast to octopamine. Our results suggest that octopamine and noradrenaline have distinct functions in olfactory information processing, in spite of their structural similarity. J. Comp. Neurol. 524:3849-3864, 2016. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Gastrópodes/citologia
Gastrópodes/metabolismo
Octopamina/metabolismo
[Mh] Termos MeSH secundário: Antagonistas Adrenérgicos alfa/farmacologia
Animais
Cálcio/metabolismo
Células Cultivadas
Sistema Nervoso Central/citologia
Sistema Nervoso Central/efeitos dos fármacos
Sistema Nervoso Central/metabolismo
Relação Dose-Resposta a Droga
Epinefrina/metabolismo
Gânglios dos Invertebrados/citologia
Gânglios dos Invertebrados/efeitos dos fármacos
Gânglios dos Invertebrados/metabolismo
Gastrópodes/efeitos dos fármacos
Potenciais da Membrana/efeitos dos fármacos
Potenciais da Membrana/fisiologia
Norepinefrina/metabolismo
Octopamina/administração & dosagem
Fentolamina/farmacologia
Filogenia
Olfato/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-Antagonists); 14O50WS8JD (Octopamine); SY7Q814VUP (Calcium); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine); Z468598HBV (Phentolamine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160518
[St] Status:MEDLINE
[do] DOI:10.1002/cne.24039


  10 / 8691 MEDLINE  
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Fotocópia
Texto completo
[PMID]:27133570
[Au] Autor:Lythgoe MP; Rhodes CJ; Ghataorhe P; Attard M; Wharton J; Wilkins MR
[Ad] Endereço:Department of Medicine, Imperial College London, W12 0NN, United Kingdom.
[Ti] Título:Why drugs fail in clinical trials in pulmonary arterial hypertension, and strategies to succeed in the future.
[So] Source:Pharmacol Ther;164:195-203, 2016 Aug.
[Is] ISSN:1879-016X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The past three decades have witnessed a welcome expansion of the therapeutic armamentarium for the management of pulmonary arterial hypertension (PAH). However, against this backdrop, there have been some notable disappointments in drug development. Here we use these as case studies to emphasize the importance of informed drug target selection, the early evaluation of dose-response relationships in human studies, and the value of the deep phenotyping of patients in clinical studies to better understand inter-individual variation in patient response. The integration of "omics" technologies and advanced clinical imaging offer the potential to reduce the risk, and so cost, of drug development in PAH and bring much needed new medicines to those patients most likely to benefit with greater efficiency.
[Mh] Termos MeSH primário: Estudos Clínicos como Assunto/métodos
Hipertensão Pulmonar/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Biomarcadores
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Combinação de Medicamentos
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/farmacologia
Hipertensão Pulmonar/patologia
Hipertensão Pulmonar/fisiopatologia
Lisurida/análogos & derivados
Lisurida/farmacologia
Fenótipo
Fentolamina/farmacologia
Proteínas Tirosina Quinases/antagonistas & inibidores
Peptídeo Intestinal Vasoativo/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Drug Combinations); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors); 0 (aviptadil); 21OJT43Q88 (dironyl); 37221-79-7 (Vasoactive Intestinal Peptide); E0QN3D755O (Lisuride); EC 2.7.10.1 (Protein-Tyrosine Kinases); Z468598HBV (Phentolamine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160503
[St] Status:MEDLINE



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