Base de dados : MEDLINE
Pesquisa : D12.776.827.137 [Categoria DeCS]
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  1 / 917 MEDLINE  
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[PMID]:28423499
[Au] Autor:Xuanfei L; Hao C; Zhujun Y; Yanming L; Jianping G
[Ad] Endereço:Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, P. R. China.
[Ti] Título:Imidazoline I2 receptor inhibitor idazoxan regulates the progression of hepatic fibrosis via Akt-Nrf2-Smad2/3 signaling pathway.
[So] Source:Oncotarget;8(13):21015-21030, 2017 Mar 28.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Liver fibrosis is a global health problem and its relationship with imidazoline I2 receptor has not been reported. This study aimed to investigate the effects and underlying mechanisms of imidazoline I2 receptor (I2R) inhibitor idazoxan (IDA) on carbon tetrachloride (CCl4)-induced liver fibrosis. In vivo liver fibrosis in mice was induced by intraperitoneally injections of CCl4 for eight weeks, and in vitro studies were performed on activated LX2 cells treated with transforming growth factor-ß (TGF-ß). Our results showed that IDA significantly improved liver inflammation, ameliorated hepatic stellate cells activation and reduced collagen accumulation by suppressing the pro-fibrogenic signaling of TGF-ß/Smad. Further investigation showed that IDA significantly balanced oxidative stress through improving the expressions and activities of anti-oxidant and detoxifying enzymes and activating Nrf2-the key defender against oxidative stress with anti-fibrotic potentials. Even more impressively, knock out of Nrf2 or suppression of Akt by perifosine (PE) eliminated the anti-oxidant and anti-fibrotic effects of IDA in vivo and in vitro, suggesting that Akt/Nrf2 constitutes a critical component of IDA's protective functions. Taken together, IDA exhibits potent effects against liver fibrosis via Akt-Nrf2-Smad2/3 signaling pathway, which suggests that specifically targeting I2R may be a potentially useful therapeutic strategy for liver fibrosis.
[Mh] Termos MeSH primário: Células Estreladas do Fígado/patologia
Idazoxano/farmacologia
Receptores de Imidazolinas/antagonistas & inibidores
Cirrose Hepática/patologia
Fator 2 Relacionado a NF-E2/fisiologia
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteína Smad2/metabolismo
Proteína Smad3/metabolismo
[Mh] Termos MeSH secundário: Antagonistas de Receptores Adrenérgicos alfa 2/farmacologia
Animais
Apoptose/efeitos dos fármacos
Tetracloreto de Carbono/toxicidade
Proliferação Celular/efeitos dos fármacos
Células Estreladas do Fígado/efeitos dos fármacos
Células Estreladas do Fígado/metabolismo
Seres Humanos
Cirrose Hepática/induzido quimicamente
Cirrose Hepática/tratamento farmacológico
Cirrose Hepática/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Estresse Oxidativo/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Antagonists); 0 (Imidazoline Receptors); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 0 (SMAD2 protein, human); 0 (SMAD3 protein, human); 0 (Smad2 Protein); 0 (Smad3 Protein); CL2T97X0V0 (Carbon Tetrachloride); EC 2.7.11.1 (AKT1 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); Y310PA316B (Idazoxan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15472


  2 / 917 MEDLINE  
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[PMID]:28332439
[Au] Autor:Vucicevic J; Popovic M; Nikolic K; Filipic S; Obradovic D; Agbaba D
[Ad] Endereço:a Department of Pharmaceutical Chemistry, Faculty of Pharmacy , University of Belgrade , Belgrade , Serbia.
[Ti] Título:Use of biopartitioning micellar chromatography and RP-HPLC for the determination of blood-brain barrier penetration of α-adrenergic/imidazoline receptor ligands, and QSPR analysis.
[So] Source:SAR QSAR Environ Res;28(3):235-252, 2017 Mar.
[Is] ISSN:1029-046X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:For this study, 31 compounds, including 16 imidazoline/α-adrenergic receptor (IRs/α-ARs) ligands and 15 central nervous system (CNS) drugs, were characterized in terms of the retention factors (k) obtained using biopartitioning micellar and classical reversed phase chromatography (log k and log k , respectively). Based on the retention factor (log k ) and slope of the linear curve (S) the isocratic parameter (φ ) was calculated. Obtained retention factors were correlated with experimental log BB values for the group of examined compounds. High correlations were obtained between logarithm of biopartitioning micellar chromatography (BMC) retention factor and effective permeability (r(log k /log BB): 0.77), while for RP-HPLC system the correlations were lower (r(log k /log BB): 0.58; r(S/log BB): -0.50; r(φ /P ): 0.61). Based on the log k retention data and calculated molecular parameters of the examined compounds, quantitative structure-permeability relationship (QSPR) models were developed using partial least squares, stepwise multiple linear regression, support vector machine and artificial neural network methodologies. A high degree of structural diversity of the analysed IRs/α-ARs ligands and CNS drugs provides wide applicability domain of the QSPR models for estimation of blood-brain barrier penetration of the related compounds.
[Mh] Termos MeSH primário: Agonistas alfa-Adrenérgicos/farmacocinética
Barreira Hematoencefálica/metabolismo
Cromatografia Líquida de Alta Pressão
Cromatografia
Receptores de Imidazolinas/agonistas
Imidazolinas/farmacocinética
[Mh] Termos MeSH secundário: Relação Quantitativa Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-Agonists); 0 (Imidazoline Receptors); 0 (Imidazolines)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170417
[Lr] Data última revisão:
170417
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170324
[St] Status:MEDLINE
[do] DOI:10.1080/1062936X.2017.1302506


  3 / 917 MEDLINE  
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[PMID]:28177562
[Au] Autor:Sato N; Saiki C; Tamiya J; Imai T; Sunada K
[Ad] Endereço:Department of Dental Anesthesiology, School of Life Dentistry at Tokyo, The Nippon Dental University, Tokyo, Japan.
[Ti] Título:Imidazoline 1 receptor activation preserves respiratory drive in spontaneously breathing newborn rats during dexmedetomidine administration.
[So] Source:Paediatr Anaesth;27(5):506-515, 2017 May.
[Is] ISSN:1460-9592
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Dexmedetomidine is an alpha-2 (α ) adrenoceptor and imidazoline 1 (I ) receptor agonist that provides sedation without loss of respiratory drive. AIMS: The aim of this study was to elucidate the involvement of α -adrenoceptor and I receptor in the cardiorespiratory changes induced by dexmedetomidine in spontaneously breathing newborn rats. METHODS: An abdominal catheter to administer drugs and three subcutaneous electrodes to record electrocardiographic data were inserted into 2- to 5-day-old Wistar rats under isoflurane anesthesia. In individual chambers, each rat was intraperitoneally administered dexmedetomidine (50 µg·kg ) followed 5 min later by normal saline or 1, 5, or 10 mg·kg atipamezole (selective α -adrenoceptor antagonist) or efaroxan (α -adrenoceptor/I receptor antagonist). Cardiorespiratory indices were recorded before and after drug administration. RESULTS: The administration of dexmedetomidine alone resulted in significant changes to most of the cardiorespiratory indices examined. The addition of 5 or 10 mg·kg atipamezole or 1 mg·kg efaroxan completely ameliorated the dexmedetomidine-associated reduction in heart rate (HR). The addition of 1 mg·kg atipamezole or 1 or 5 mg·kg efaroxan completely ameliorated the dexmedetomidine-associated reduction in respiratory frequency. Mean inspiratory flow (V /T ; V is tidal volume and T is inspiratory time), which is an index of respiratory drive, was not significantly affected by the administration of dexmedetomidine alone (P = 0.273) or dexmedetomidine + atipamezole (P = 0.605, 0.153, 0.138 for 1, 5, 10 mg·kg atipamezole, respectively); however, it was significantly decreased after the administration of dexmedetomidine + efaroxan (P = 0.029, <0.001, <0.001 for 1, 5, 10 mg·kg efaroxan, respectively). CONCLUSIONS: Our results suggest that in newborn rats undergoing dexmedetomidine sedation, the α -adrenoceptor, but not I receptor, is involved in the regulation of HR and respiratory frequency, and that activation of the I receptor plays a major role in the maintenance of respiratory drive.
[Mh] Termos MeSH primário: Agonistas de Receptores Adrenérgicos alfa 2/farmacologia
Dexmedetomidina/farmacologia
Impulso (Psicologia)
Hipnóticos e Sedativos/farmacologia
Receptores de Imidazolinas/agonistas
Respiração/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antagonistas de Receptores Adrenérgicos alfa 2/farmacologia
Animais
Animais Recém-Nascidos
Temperatura Corporal
Eletrocardiografia/efeitos dos fármacos
Feminino
Frequência Cardíaca/efeitos dos fármacos
Pletismografia
Gravidez
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Agonists); 0 (Adrenergic alpha-2 Receptor Antagonists); 0 (Hypnotics and Sedatives); 0 (Imidazoline Receptors); 0 (imidazoline I1 receptors); 67VB76HONO (Dexmedetomidine)
[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:170209
[St] Status:MEDLINE
[do] DOI:10.1111/pan.13107


  4 / 917 MEDLINE  
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[PMID]:28131840
[Au] Autor:Chang C; Wei W; Han D; Meng J; Zhu F; Xiao Y; Wu G; Shi X; Zhang L
[Ad] Endereço:Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
[Ti] Título:Expression of Nischarin negatively correlates with estrogen receptor and alters apoptosis, migration and invasion in human breast cancer.
[So] Source:Biochem Biophys Res Commun;484(3):536-542, 2017 Mar 11.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nischarin, a novel integrin binding protein, has been demonstrated its negative effects on cell migration and invasion. However, the biological role of Nischarin in breast cancer has not been fully elucidated yet. Our study aimed to analyze the association between Nischarin expression and clinical features of breast cancer patients, and further investigate the role of Nischarin in breast cancer cells apoptosis, migration and invasion. Results showed that Nischarin expression was significantly lower in breast cancer tissues (37.8%, 23/67) than in normal tissues (61.8%, 21/34; P < 0.05), and the expression of Nischarin significantly negatively correlated with estrogen receptor status. Similarly, Nischarin expression was highest in normal breast cell line HBL-100 while triple-negative breast cancer cell line MDA-MB-231 had the lowest expression of Nischarin. Further experiments demonstrated that overexpression of Nischarin may induce apoptosis, and inhibit cell migration and invasion. The present data confirmed that Nishcharin might be a novel tumor suppressor and plays an important role in breast cancer cell apoptosis and metastasis, which can be used as a potential therapeutic target for breast cancer treatment.
[Mh] Termos MeSH primário: Apoptose
Neoplasias da Mama/metabolismo
Neoplasias da Mama/patologia
Movimento Celular
Receptores de Imidazolinas/metabolismo
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Receptores Estrogênicos/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Invasividade Neoplásica
Estatística como Assunto
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Imidazoline Receptors); 0 (Intracellular Signaling Peptides and Proteins); 0 (NISCH protein, human); 0 (Receptors, Estrogen)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170130
[St] Status:MEDLINE


  5 / 917 MEDLINE  
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[PMID]:28029766
[Au] Autor:Abás S; Erdozain AM; Keller B; Rodríguez-Arévalo S; Callado LF; García-Sevilla JA; Escolano C
[Ad] Endereço:Laboratory of Medicinal Chemistry (Associated Unit to CSIC), Department of Pharmacology, Toxicology and Medicinal Chemistry, Faculty of Pharmacy and Food Sciences, and Institute of Biomedicine (IBUB), University of Barcelona , Av. Joan XXIII 27-31, E-08028 Barcelona, Spain.
[Ti] Título:Neuroprotective Effects of a Structurally New Family of High Affinity Imidazoline I Receptor Ligands.
[So] Source:ACS Chem Neurosci;8(4):737-742, 2017 Apr 19.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The imidazoline I receptors (I -IRs) are widely distributed in the brain, and I -IR ligands may have therapeutic potential as neuroprotective agents. Since structural data for I -IR remains unknown, the discovery of selective I -IR ligands devoid of α -adrenoceptor (α -AR) affinity is likely to provide valuable tools in defining the pharmacological characterization of these receptors. We report the pharmacological characterization of a new family of (2-imidazolin-4-yl)phosphonates. Radioligand binding studies showed that they displayed a higher affinity for I -IRs than idazoxan, and high I /α selectivity. In vivo studies in mice showed that acute treatments with 1b and 2c significantly increased p-FADD/FADD ratio (an index of cell survival) in the hippocampus when compared with vehicle-treated controls. Additionally, acute and repeated treatments with 2c, but not with 1b, markedly reduced hippocampal p35 cleavage into neurotoxic p25. The present results indicate a neuroprotective potential of (2-imidazolin-4-yl)phosphonates acting at I -IRs.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Receptores de Imidazolinas/agonistas
Imidazolinas/farmacologia
Fármacos Neuroprotetores/farmacologia
[Mh] Termos MeSH secundário: Animais
Imidazolinas/síntese química
Imidazolinas/química
Ligantes
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Imidazoline Receptors); 0 (Imidazolines); 0 (Ligands); 0 (Neuroprotective Agents); 0 (imidazoline receptor 2)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161229
[St] Status:MEDLINE
[do] DOI:10.1021/acschemneuro.6b00426


  6 / 917 MEDLINE  
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[PMID]:27873165
[Au] Autor:Fehér Á; Tóth VE; Al-Khrasani M; Balogh M; Lázár B; Helyes Z; Gyires K; Zádori ZS
[Ad] Endereço:Department of Pharmacology and Pharmacotherapy, Faculty of Medicine, Semmelweis University, Nagyvárad tér 4, Budapest, 1089, Hungary.
[Ti] Título:Analysing the effect of I imidazoline receptor ligands on DSS-induced acute colitis in mice.
[So] Source:Inflammopharmacology;25(1):107-118, 2017 Feb.
[Is] ISSN:1568-5608
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Imidazoline receptors (IRs) have been recognized as promising targets in the treatment of numerous diseases; and moxonidine and rilmenidine, agonists of I -IRs, are widely used as antihypertensive agents. Some evidence suggests that IR ligands may induce anti-inflammatory effects acting on I -IRs or other molecular targets, which could be beneficial in patients with inflammatory bowel disease (IBD). On the other hand, several IR ligands may stimulate also alpha -adrenoceptors, which were earlier shown to inhibit, but in more recent studies to rather aggravate colitis. Hence, this study aimed to analyse for the first time the effect of various I -IR ligands on intestinal inflammation. Colitis was induced in C57BL/6 mice by adding dextran sulphate sodium (DSS) to the drinking water for 7 days. Mice were treated daily with different IR ligands: moxonidine and rilmenidine (I -IR agonists), AGN 192403 (highly selective I -IR ligand, putative antagonist), efaroxan (I -IR antagonist), as well as with the endogenous IR agonists agmatine and harmane. It was found that moxonidine and rilmenidine at clinically relevant doses, similarly to the other IR ligands, do not have a significant impact on the macroscopic and histological signs of DSS-evoked inflammation. Likewise, colonic myeloperoxidase and serum interleukin-6 levels remained unchanged in response to these agents. Thus, our study demonstrates that imidazoline ligands do not influence significantly the severity of DSS-colitis in mice and suggest that they probably neither affect the course of IBD in humans. However, the translational value of these findings needs to be verified with other experimental colitis models and human studies.
[Mh] Termos MeSH primário: Colite/tratamento farmacológico
Colite/metabolismo
Sulfato de Dextrana/toxicidade
Receptores de Imidazolinas/metabolismo
Imidazolinas/metabolismo
Imidazolinas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Colite/induzido quimicamente
Feminino
Ligantes
Camundongos
Camundongos Endogâmicos C57BL
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Imidazoline Receptors); 0 (Imidazolines); 0 (Ligands); 0 (imidazoline I1 receptors); 9042-14-2 (Dextran Sulfate)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161123
[St] Status:MEDLINE
[do] DOI:10.1007/s10787-016-0299-7


  7 / 917 MEDLINE  
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[PMID]:27836117
[Au] Autor:Keller B; García-Sevilla JA
[Ad] Endereço:Laboratori de Neurofarmacologia, IUNICS/IdISPa, Universitat de les Illes Balears (UIB), Palma de Mallorca, Spain; Redes Temáticas de Investigación Cooperativa en Salud-Red de Trastornos Adictivos (RETICS-RTA), ISCIII, Madrid, Spain.
[Ti] Título:Dysregulation of IRAS/nischarin and other potential I -imidazoline receptors in major depression postmortem brain: Downregulation of basal contents by antidepressant drug treatments.
[So] Source:J Affect Disord;208:646-652, 2017 Jan 15.
[Is] ISSN:1573-2517
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Major depressive disorder (MDD) has been associated with altered brain densities of imidazoline receptors (I -IR and I -IR types). METHODS: The contents of potential I -IR IRAS/nischarin (167kDa) and, for comparison, those of I - (85kDa) and I - (45kDa and 30kDa) IR proteins were quantified by western blotting in postmortem prefrontal cortex (PFC/BA9) of antidepressant-free ([MDD(-)], n=9) and antidepressant-treated ([MDD(+)], n=12) subjects and matched controls (n=19). RESULTS: In MDD, regardless of antidepressant treatment (n=21), IRAS/nischarin was not altered in PFC/BA9. However, the content of IRAS/nischarin was found modestly and not significantly increased (+19%, p=0.075) in MDD(-) and significantly decreased (-24%, p=0.001) in MDD(+), revealing that basal I -IR content was downregulated by antidepressants. Putative 85kDa I -IR was upregulated (+35%, p=0.035) in MDD(-) but it was not reduced (-14%, p=0.37) in MDD(+). There was a positive correlation (r=0.33, p=0.037, n=40) between the contents of IRAS/nischarin and 85kDa IR proteins in PFC/BA9 (control and MDD subjects). In MDD and regardless of antidepressants, the content of cortical 45kDa I -IR was increased (+31%, p=0.006) and that of 30kDa I -IR decreased (-14%, p=0.002), indicating basal dysregulations of these potential IRs. LIMITATIONS: MDD(+) subjects had been treated with a variety of antidepressant drugs. The results must be understood in the context of suicide victims with MDD. CONCLUSIONS: The dysregulation of IRAS/nischarin in depressed brains is a major novel finding that supports a role of this potential I -IR in the neurobiology of MDD and in the molecular mechanisms of antidepressant drugs.
[Mh] Termos MeSH primário: Encéfalo/efeitos dos fármacos
Transtorno Depressivo Maior/tratamento farmacológico
Receptores de Imidazolinas/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Antidepressivos/uso terapêutico
Autopsia
Encéfalo/metabolismo
Estudos de Casos e Controles
Regulação para Baixo/efeitos dos fármacos
Feminino
Seres Humanos
Receptores de Imidazolinas/metabolismo
Masculino
Meia-Idade
Córtex Pré-Frontal/efeitos dos fármacos
Suicídio
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidepressive Agents); 0 (Imidazoline Receptors); 0 (imidazoline I1 receptors)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161113
[St] Status:MEDLINE


  8 / 917 MEDLINE  
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Antunes, Edson
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[PMID]:27729248
[Au] Autor:Ferreira RB; de Oliveira MG; Antunes E; Almeida WP; Ibrahim BM; Abdel-Rahman AA
[Ad] Endereço:Institute of Chemistry, University of Campinas, PO Box 6194, ZC 13083-970 Campinas, SP, Brazil.
[Ti] Título:New 2-Aminothiazoline derivatives lower blood pressure of spontaneously hypertensive rats (SHR) via I -imidazoline and alpha-2 adrenergic receptors activation.
[So] Source:Eur J Pharmacol;791:803-810, 2016 Nov 15.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:2-Aminothiazolines share an isosteric relationship with imidazolines and oxazolines with antihypertensive activity mainly mediated by the imidazoline I -receptor. In the present work, we have prepared five aminothiazolines, following a previously described synthetic pathway. Aminothiazolines derived from dicyclopropylmethylamine (ATZ1) and cyclohexylamine (3) are unprecedented in the literature. Competitive radioligand assay was carried out with all synthetic compounds, and the I receptor affinity in comparison to rilmenidine in PC12 cells was determined. Surprisingly, the rilmenidine isoster (ATZ1) showed no I -receptor interaction. Diethyl (ATZ4) and 2-ethyl-hexylamine (ATZ5) derivatives bind to the receptor with 11.98 and 10.94nmol/l, respectively. These compounds were selected for in vivo experiments. Both compounds reduced the blood pressure of spontaneously hypertensive rats (SHR). The hypotensive effect of these compounds was abrogated in the presence of α adrenergic (yohimbine) and I (efaroxan) receptor antagonists suggesting that both aminothiazolines bind to the adrenergic and imidazoline receptors. Lipinski's descriptors of the synthesized aminothiazolines were calculated and are similar to the known imidazoline I receptor ligands. 3D-Similarity between ATZ5 and agmatine, the natural imidazoline receptor ligand, was also observed.
[Mh] Termos MeSH primário: Anti-Hipertensivos/química
Anti-Hipertensivos/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Receptores de Imidazolinas/metabolismo
Receptores Adrenérgicos alfa 2/metabolismo
Tiazóis/química
Tiazóis/farmacologia
[Mh] Termos MeSH secundário: Animais
Benzofuranos/farmacologia
Imidazóis/farmacologia
Modelos Moleculares
Conformação Molecular
Células PC12
Ratos
Ratos Endogâmicos SHR
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Benzofurans); 0 (Imidazoles); 0 (Imidazoline Receptors); 0 (Receptors, Adrenergic, alpha-2); 0 (Thiazoles); 0 (imidazoline I1 receptors); 5JC2YZG56Q (2-aminothiazoline); G00490L21H (efaroxan)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161013
[St] Status:MEDLINE


  9 / 917 MEDLINE  
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[PMID]:27320860
[Au] Autor:Kim YH; Jeong JH; Ahn DS; Chung S
[Ad] Endereço:Department of Physiology, Brain Korea 21 Plus Project for Medical Science, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.
[Ti] Título:Agmatine suppresses peripheral sympathetic tone by inhibiting N-type Ca(2+) channel activity via imidazoline I2 receptor activation.
[So] Source:Biochem Biophys Res Commun;477(3):406-12, 2016 08 26.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Agmatine, a putative endogenous ligand of imidazoline receptors, suppresses cardiovascular function by inhibiting peripheral sympathetic tone. However, the molecular identity of imidazoline receptor subtypes and its cellular mechanism underlying the agmatine-induced sympathetic suppression remains unknown. Meanwhile, N-type Ca(2+) channels are important for the regulation of NA release in the peripheral sympathetic nervous system. Therefore, it is possible that agmatine suppresses NA release in peripheral sympathetic nerve terminals by inhibiting Ca(2+) influx through N-type Ca(2+) channels. We tested this hypothesis by investigating agmatine effect on electrical field stimulation (EFS)-evoked contraction and NA release in endothelium-denuded rat superior mesenteric arterial strips. We also investigated the effect of agmatine on the N-type Ca(2+) current in superior cervical ganglion (SCG) neurons in rats. Our study demonstrates that agmatine suppresses peripheral sympathetic outflow via the imidazoline I2 receptor in rat mesenteric arteries. In addition, the agmatine-induced suppression of peripheral vascular sympathetic tone is mediated by modulating voltage-dependent N-type Ca(2+) channels in sympathetic nerve terminals. These results suggest a potential cellular mechanism for the agmatine-induced suppression of peripheral sympathetic tone. Furthermore, they provide basic and theoretical information regarding the development of new agents to treat hypertension.
[Mh] Termos MeSH primário: Agmatina/farmacologia
Bloqueadores dos Canais de Cálcio/farmacologia
Canais de Cálcio Tipo N/efeitos dos fármacos
Receptores de Imidazolinas/agonistas
Sistema Nervoso Simpático/efeitos dos fármacos
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Estimulação Elétrica
Técnicas In Vitro
Masculino
Artérias Mesentéricas/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Calcium Channel Blockers); 0 (Calcium Channels, N-Type); 0 (Imidazoline Receptors); 70J407ZL5Q (Agmatine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160621
[St] Status:MEDLINE


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[PMID]:27282217
[Au] Autor:Cabral KA; Andrade CA
[Ad] Endereço:Graduate Program in Physiology of the Brazilian Physiological Society, Unifal-MG, Alfenas, MG, Brazil.
[Ti] Título:Importance of the lateral parabrachial nucleus to sodium balance in fluid-depleted rats.
[So] Source:Neurosci Res;111:41-7, 2016 Oct.
[Is] ISSN:1872-8111
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:The lateral parabrachial nucleus (LPBN) exerts an important inhibitory influence for the control of sodium and water intake. However, the importance of LPBN on renal responses and cardiovascular changes during extracellular dehydration are still unknown. Here we investigated the effects of bilateral injections of moxonidine (alpha2-adrenergic and imidazoline receptor agonist) on renal and cardiovascular changes in fluid-depleted rats. Male Wistar rats (n=4-8 per group) with bilateral stainless steel guide-cannulas implanted into the LPBN were treated with subcutaneous furosemide (10mg/kg)+captopril (5mg/kg) to induce fluid depletion. Forty-five min later vehicle or moxonidine (0.5nmol/0.2µl) were bilaterally injected into the LPBN. In fluid-depleted rats, moxonidine produced strong 0.3M NaCl and water intake without noticeable changes in cardiovascular parameters. Moxonidine did not change sodium excretion (488±135, vs. vehicle: 376±75µEq/1h) or urinary volume (2.5±0.7, vs. vehicle: 2.5±0.3ml/1h) in fluid-depleted rats without access to fluids for rehydration. However, moxonidine decreased natriuresis (462±127, vs. vehicle: 888±122µEq/1h) and diuresis (2.5±0.5, vs. vehicle: 4.5±0.5ml/1h) in fluid-depleted rats submitted to i.g. rehydration. These data suggest that alpha2-adrenergic mechanism of the LPBN facilitates sodium/water retention and body fluid volume expansion during extracellular dehydration.
[Mh] Termos MeSH primário: Desidratação/fisiopatologia
Núcleos Parabraquiais/fisiologia
Sódio/fisiologia
Equilíbrio Hidroeletrolítico
[Mh] Termos MeSH secundário: Agonistas de Receptores Adrenérgicos alfa 2/farmacologia
Animais
Pressão Sanguínea/efeitos dos fármacos
Líquidos Corporais/fisiologia
Desidratação/urina
Diuréticos/farmacologia
Ingestão de Líquidos
Furosemida/farmacologia
Receptores de Imidazolinas/agonistas
Masculino
Natriurese
Ratos Wistar
Sódio/urina
Urina
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-2 Receptor Agonists); 0 (Diuretics); 0 (Imidazoline Receptors); 7LXU5N7ZO5 (Furosemide); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170113
[Lr] Data última revisão:
170113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160611
[St] Status:MEDLINE



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