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[PMID]:28453961
[Au] Autor:Sharma D; Bhattacharya P; Kalia K; Tiwari V
[Ad] Endereço:Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research (NIPER)-Ahmedabad, Gandhinagar 382355, Gujarat, India.
[Ti] Título:Diabetic nephropathy: New insights into established therapeutic paradigms and novel molecular targets.
[So] Source:Diabetes Res Clin Pract;128:91-108, 2017 Jun.
[Is] ISSN:1872-8227
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Diabetic nephropathy is one of the most prevalent microvascular complication in patients suffering from diabetes and is reported to be the major cause of renal failure when compared to any other kidney disease. Currently, available therapies provide only symptomatic relief and unable to treat the underlying pathophysiology of diabetic nephropathy. This review will explore new insights into the established therapeutic paradigms targeting oxidative stress, inflammation and endoplasmic reticulum stress with the focus on recent clinical developments. Apart from this, the involvement of novel cellular and molecular mechanisms including the role of endothelin-receptor antagonists, Wnt signaling pathway, epigenetics and micro RNA is also discussed so that key molecular switches involved in the pathogenesis of diabetic nephropathy can be identified. Elucidating new molecular pathways will help in the development of novel therapeutics for the prevention and treatment of diabetic nephropathy.
[Mh] Termos MeSH primário: Nefropatias Diabéticas/fisiopatologia
Endotelinas/metabolismo
Epigenômica/métodos
Inflamação/complicações
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Endothelins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171212
[Lr] Data última revisão:
171212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:28781261
[Au] Autor:Gumanova NG; Klimushina MV; Gavrilova NE; Metelskaya VA
[Ad] Endereço:National Research Center for Preventive Medicine.
[Ti] Título:[Combined markers of initial stages of coronary atherosclerosis].
[Ti] Título:Kombinirovannye markery nachal'noi stadii ateroskleroza koronarnykh arterii..
[So] Source:Biomed Khim;63(3):272-277, 2017 May.
[Is] ISSN:2310-6972
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Abnormalities in energy metabolism and endothelial dysfunction contribute to signaling processes associated with atherogenesis. The goal of our study was to develop diagnostic tests based on endothelial functional markers and adiponectin to differentiate early stages of coronary lesions during atherogenesis. The cohort included male and female patients from 25 to 86 years of age. All subjects underwent coronary angiography and severity of coronary lesions was quantified by the Gensini score that assigns points depending on location and extent of the lesions. We have estimated associations between the Gensini score and some known primary and secondary diagnostic parameters and have found that the ratio of serum levels of adiponectin to endothelin strongly correlates with severity of coronary lesions and can be used for differentiation of male patients lacking coronary atherosclerosis (despite symptoms of ischemic heart disease) from patients that have severe coronary lesions. Predictive power of adiponectin to endothelin ratio did not depend on drug therapy.
[Mh] Termos MeSH primário: Adiponectina/sangue
Aterosclerose/sangue
Doença da Artéria Coronariana/sangue
Endotelinas/sangue
Isquemia Miocárdica/sangue
[Mh] Termos MeSH secundário: Adiponectina/genética
Adulto
Idoso
Idoso de 80 Anos ou mais
Aterosclerose/diagnóstico por imagem
Aterosclerose/genética
Aterosclerose/patologia
Biomarcadores/sangue
Angiografia Coronária
Doença da Artéria Coronariana/diagnóstico por imagem
Doença da Artéria Coronariana/genética
Doença da Artéria Coronariana/patologia
Endotelinas/genética
Feminino
Expressão Gênica
Seres Humanos
Masculino
Meia-Idade
Isquemia Miocárdica/diagnóstico por imagem
Isquemia Miocárdica/genética
Isquemia Miocárdica/patologia
Curva ROC
Índice de Gravidade de Doença
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ADIPOQ protein, human); 0 (Adiponectin); 0 (Biomarkers); 0 (Endothelins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170912
[Lr] Data última revisão:
170912
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE
[do] DOI:10.18097/PBMC20176303272


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[PMID]:28637196
[Au] Autor:Cho HJ; Heo W; Han JW; Lee YH; Park JM; Kang MJ; Yoon JH; Lee MG; Kim CH; Kim JY
[Ad] Endereço:Department of Otorhinolaryngology, Yonsei University College of Medicine, Seoul, Korea.
[Ti] Título:Chronological Change of Right Ventricle by Chronic Intermittent Hypoxia in Mice.
[So] Source:Sleep;40(8), 2017 Aug 01.
[Is] ISSN:1550-9109
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Study Objective: No studies have investigated sequential changes in the heart on magnetic resonance imaging (MRI), along with observation of functional lung phenotypes and genetics, over the duration of chronic intermittent hypoxia (CIH). We investigated chronological changes in heart and lung phenotypes after CIH using a mouse model to provide new insights into the pathophysiology of sleep apnea-induced cardiovascular disease. Methods: C57BL/6J adult male mice were randomized to 4 or 8 weeks of CIH. Cardiac cine-MRI images were analyzed to assess functional parameters of right ventricle (RV). Histopathological features of myocytes and pulmonary vessels, as well as genes involved in the endothelin (ET) system, were investigated. Results: Function of the RV reduced significantly at 4 weeks and continuously decreased following another 4 weeks of CIH, although the rate of decrease was attenuated. Notably, persistence of reduced ejection fraction and end-systole RV wall thickness (WT) and increases in the ET system of the lungs and blood strongly implied the development of pulmonary hypertension after 8 weeks of CIH. Conclusions: RV dysfunction with reduced end-systole RV WT could be a late phenotype in long-standing CIH and possibly also in obstructive sleep apnea.
[Mh] Termos MeSH primário: Ventrículos do Coração/patologia
Hipóxia/patologia
[Mh] Termos MeSH secundário: Animais
Doença Crônica
Modelos Animais de Doenças
Endotelinas/metabolismo
Pulmão/irrigação sanguínea
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Células Musculares/metabolismo
Células Musculares/patologia
Apneia Obstrutiva do Sono/metabolismo
Apneia Obstrutiva do Sono/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1093/sleep/zsx103


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[PMID]:28632730
[Au] Autor:Kim R; Chiorean EG; Amin M; Rocha-Lima CMS; Gandhi J; Harris WP; Song T; Portnoy D
[Ad] Endereço:Department of Gastrointestinal Oncology, H. Lee Moffitt Cancer Center &Research Institute, 12902 Magnolia Drive FOB-2, Tampa, FL 33612, USA.
[Ti] Título:Phase 2 study of combination SPI-1620 with docetaxel as second-line advanced biliary tract cancer treatment.
[So] Source:Br J Cancer;117(2):189-194, 2017 Jul 11.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: This multicentre, open-label study evaluated the efficacy and safety of SPI-1620, an analogue of endothelin-1, administered in combination with docetaxel as second-line treatment for patients with advanced biliary tract cancer (ABTC). METHODS: Eligible patients received continuous cycles of combination therapy with SPI-1620 (11 µg m ) and docetaxel (75 mg m ) intravenously every 3 weeks until disease progression (PD) or intolerable toxicity. Tumour response was evaluated using computed tomography or magnetic resonance imaging every 2 cycles (6 weeks). The primary efficacy end point was progression-free survival (PFS); secondary end points included overall response rate (ORR), duration of response, and overall survival (OS) that were estimated using the Kaplan-Meier method. RESULTS: Of the 30 enrolled patients, 25 patients had qualifying events (PD or death), 1 patient was nonevaluable, and 4 patients were censored at the time of their last tumour assessment. Our primary end point of PFS ⩾5 months was not reached. Median PFS was 2.6 months (95% confidence interval (CI): 1.4-2.8), ranging from 0.7 to 8.4 months. The ORR was 10.3% (95% CI: 0.02-0.27). Eleven additional patients achieved stable disease. The OS was 4.87 months. The most common grade 3-4 toxicities were febrile neutropenia and neutropenia. CONCLUSIONS: The addition of docetaxel to SPI-1620 in second-line ABTC did not meet the pre-specified primary end point of PFS ⩾5 months in unselected patient population.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/administração & dosagem
Neoplasias do Sistema Biliar/tratamento farmacológico
Endotelinas/administração & dosagem
Fragmentos de Peptídeos/administração & dosagem
Taxoides/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Neoplasias do Sistema Biliar/patologia
Intervalo Livre de Doença
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/classificação
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/patologia
Endotelinas/efeitos adversos
Feminino
Seres Humanos
Masculino
Meia-Idade
Recidiva Local de Neoplasia/tratamento farmacológico
Recidiva Local de Neoplasia/patologia
Fragmentos de Peptídeos/efeitos adversos
Taxoides/efeitos adversos
Resultado do Tratamento
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Endothelins); 0 (Peptide Fragments); 0 (Taxoids); 11X778QIZS (IRL 1620); 15H5577CQD (docetaxel)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170621
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2017.160


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[PMID]:28488307
[Au] Autor:Sun YY; Zhang WJ; Dong CL; Zhang XF; Ji J; Wang X; Wang L; Hu WL; Du WJ; Cui CL; Zhang CF; Li F; Wang CZ; Yuan CS
[Ad] Endereço:State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, JS, 210009, China.
[Ti] Título:Baicalin Alleviates Nitroglycerin-induced Migraine in Rats via the Trigeminovascular System.
[So] Source:Phytother Res;31(6):899-905, 2017 Jun.
[Is] ISSN:1099-1573
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Migraine is a common neurological disorder with a serious impact on quality of life. The aim of this study was to explore the effect of baicalin on nitroglycerin-induced migraine rats. We carried out a behavioral research within 2 h post-nitroglycerin injection, and blood samples were drawn for measurements of nitric oxide (NO), calcitonin gene-related peptide, and endothelin (ET) levels. Immunohistochemistry was adopted to detect the activation of C-fos immunoreactive neurons in periaqueductal gray. The number, area size, and integrated optical density of C-fos positive cells were measured using Image-Pro Plus. As a result, baicalin administration (0.22 mm/kg) alleviated pain responses of migraine rats. It profoundly decreased NO and calcitonin gene-related peptide levels, increased ET levels, and rebuilt the NO/ET balance in migraine rats. Besides, baicalin pretreatment significantly reduced the number, the stained area size, and integrated optical density value of C-fos positive cells. In brief, this paper supports the possibility of baicalin as a potential migraine pharmacotherapy. Copyright © 2017 John Wiley & Sons, Ltd.
[Mh] Termos MeSH primário: Flavonoides/farmacologia
Transtornos de Enxaqueca/tratamento farmacológico
Nitroglicerina/efeitos adversos
Núcleo Inferior Caudal do Nervo Trigêmeo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Peptídeo Relacionado com Gene de Calcitonina/metabolismo
Endotelinas/metabolismo
Feminino
Masculino
Transtornos de Enxaqueca/induzido quimicamente
Neurônios/efeitos dos fármacos
Óxido Nítrico/metabolismo
Proteínas Proto-Oncogênicas c-fos/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelins); 0 (Flavonoids); 0 (Proto-Oncogene Proteins c-fos); 31C4KY9ESH (Nitric Oxide); 347Q89U4M5 (baicalin); 83652-28-2 (Calcitonin Gene-Related Peptide); G59M7S0WS3 (Nitroglycerin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170511
[St] Status:MEDLINE
[do] DOI:10.1002/ptr.5811


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[PMID]:28323184
[Au] Autor:Hendrix P; Foreman PM; Starke RM; Harrigan MR; Fisher WS; Vyas NA; Lipsky RH; Lin M; Walters BC; Tubbs RS; Shoja MM; Pittet JF; Mathru M; Griessenauer CJ
[Ad] Endereço:Department of Neurosurgery, Saarland University Medical Center and Saarland University Faculty of Medicine, Homburg/Saar, Germany. Electronic address: hendrix.philipp@gmail.com.
[Ti] Título:Associations of Endothelin Polymorphisms and Aneurysm Size at Time of Rupture.
[So] Source:World Neurosurg;102:253-257, 2017 Jun.
[Is] ISSN:1878-8769
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Aneurysm size is an important risk factor for aneurysm rupture. The pathophysiologic mechanisms underlying aneurysm growth remain poorly understood. Endothelin signaling is critical for cerebrovascular blood flow regulation. The influence of endothelin single nucleotide polymorphisms (SNPs) on aneurysm size at the time of rupture has not been previously investigated. METHODS: Eight common endothelin SNPs were assessed using blood samples from aneurysmal subarachnoid hemorrhage (aSAH) patients enrolled in the Cerebral Aneurysm Renin Angiotensin System study, a prospective, 2-center study that enrolled aSAH patients and controls in the United States from 2012-2015. Genetic evaluation was performed using 5'exonnuclease (Taqman) genotyping assays. Associations of endothelin SNPs and aneurysm size were analyzed. RESULTS: One-hundred and forty-nine blood samples from aSAH patients were available for analysis. There was a dominant effect of the G allele of the endothelin receptor type A (EDNRA) SNP rs5335 on aneurysm size ≥7 mm (odds ratio = 2.740, 95% confidence interval 1.039-7.228, P = 0.042) along with associations with race and presence of additional aneurysms. The other endothelin SNPs were not associated with aneurysm size. CONCLUSIONS: The EDNRA SNP rs5335 was independently associated with aneurysms ≥7 mm in size at the time of rupture. Patients with cerebral aneurysms also carrying the G allele of EDNRA SNP rs5335 may develop larger aneurysms before rupture.
[Mh] Termos MeSH primário: Aneurisma Roto/genética
Endotelinas/genética
Predisposição Genética para Doença/genética
Polimorfismo de Nucleotídeo Único/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Aneurisma Roto/diagnóstico por imagem
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Fatores de Risco
Tomógrafos Computadorizados
Estados Unidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Endothelins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170322
[St] Status:MEDLINE


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[PMID]:28264495
[Au] Autor:Bakrania B; Duncan J; Warrington JP; Granger JP
[Ad] Endereço:Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216, USA. bbakrania@umc.edu.
[Ti] Título:The Endothelin Type A Receptor as a Potential Therapeutic Target in Preeclampsia.
[So] Source:Int J Mol Sci;18(3), 2017 Feb 28.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Preeclampsia (PE) is a disorder of pregnancy typically characterized by new onset hypertension after gestational week 20 and proteinuria. Although PE is one of the leading causes of maternal and perinatal morbidity and death worldwide, the mechanisms of the pathogenesis of the disease remain unclear and treatment options are limited. However, there is increasing evidence to suggest that endothelin-1 (ET-1) plays a critical role in the pathophysiology of PE. Multiple studies report that ET-1 is increased in PE and some studies report a positive correlation between ET-1 and the severity of symptoms. A number of experimental models of PE are also associated with elevated tissue levels of prepro ET-1 mRNA. Moreover, experimental models of PE (placental ischemia, sFlt-1 infusion, Tumor necrosis factor (TNF) -α infusion, and Angiotensin II type 1 receptor autoantibody (AT1-AA) infusion) have proven to be susceptible to Endothelin Type A (ET ) receptor antagonism. While the results are promising, further work is needed to determine whether ET antagonists could provide an effective therapy for the management of preeclampsia.
[Mh] Termos MeSH primário: Antagonistas do Receptor de Endotelina A/farmacologia
Antagonistas do Receptor de Endotelina A/uso terapêutico
Pré-Eclâmpsia/tratamento farmacológico
Pré-Eclâmpsia/metabolismo
Receptor de Endotelina A/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Endotelinas/genética
Endotelinas/metabolismo
Endotélio/efeitos dos fármacos
Endotélio/metabolismo
Feminino
Seres Humanos
Terapia de Alvo Molecular
Pré-Eclâmpsia/diagnóstico
Pré-Eclâmpsia/etiologia
Gravidez
Receptor de Endotelina A/genética
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Endothelin A Receptor Antagonists); 0 (Endothelins); 0 (Receptor, Endothelin A)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170308
[St] Status:MEDLINE


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[PMID]:28223322
[Au] Autor:Vercauteren M; Trensz F; Pasquali A; Cattaneo C; Strasser DS; Hess P; Iglarz M; Clozel M
[Ad] Endereço:Drug Discovery Department, Actelion Pharmaceuticals Ltd., Allschwil, Switzerland.
[Ti] Título:Endothelin ET Receptor Blockade, by Activating ET Receptors, Increases Vascular Permeability and Induces Exaggerated Fluid Retention.
[So] Source:J Pharmacol Exp Ther;361(2):322-333, 2017 May.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endothelin (ET) receptor antagonists have been associated with fluid retention. It has been suggested that, of the two endothelin receptor subtypes, ET receptors should not be blocked, because of their involvement in natriuresis and diuresis. Surprisingly, clinical data suggest that ET -selective antagonists pose a greater risk of fluid overload than dual antagonists. The purpose of this study was to evaluate the contribution of each endothelin receptor to fluid retention and vascular permeability in rats. Sitaxentan and ambrisentan as ET -selective antagonists and bosentan and macitentan as dual antagonists were used as representatives of each class, respectively. ET -selective antagonism caused a dose-dependent hematocrit/hemoglobin decrease that was prevented by ET -selective receptor antagonism. ET -selective antagonism led to a significant blood pressure reduction, plasma volume expansion, and a greater increase in vascular permeability than dual antagonism. Isolated vessel experiments showed that ET -selective antagonism increased vascular permeability via ET receptor overstimulation. Acutely, ET -selective but not dual antagonism activated sympathetic activity and increased plasma arginine vasopressin and aldosterone concentrations. The hematocrit/hemoglobin decrease induced by ET -selective antagonism was reduced in Brattleboro rats and in Wistar rats treated with an arginine vasopressin receptor antagonist. Finally, the decrease in hematocrit/hemoglobin was larger in the venous than in the arterial side, suggesting fluid redistribution. In conclusion, by activating ET receptors, endothelin receptor antagonists (particularly ET -selective antagonists) favor edema formation by causing: 1) fluid retention resulting from arginine vasopressin and aldosterone activation secondary to vasodilation, and 2) increased vascular permeability. Plasma volume redistribution may explain the clinical observation of a hematocrit/hemoglobin decrease even in the absence of signs of fluid retention.
[Mh] Termos MeSH primário: Permeabilidade Capilar/efeitos dos fármacos
Antagonistas dos Receptores de Endotelina/farmacologia
Receptor de Endotelina A/metabolismo
Receptor de Endotelina B/metabolismo
[Mh] Termos MeSH secundário: Aldosterona/metabolismo
Animais
Antagonistas de Receptores de Hormônios Antidiuréticos/farmacologia
Arginina Vasopressina/metabolismo
Endotelinas/metabolismo
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/metabolismo
Hematócrito/métodos
Hemoglobinas/metabolismo
Masculino
Fenilpropionatos/farmacologia
Piridazinas/farmacologia
Pirimidinas/farmacologia
Ratos
Ratos Brattleboro
Ratos Wistar
Receptores de Vasopressinas/metabolismo
Sulfonamidas/farmacologia
Vasodilatação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antidiuretic Hormone Receptor Antagonists); 0 (Endothelin Receptor Antagonists); 0 (Endothelins); 0 (Hemoglobins); 0 (Phenylpropionates); 0 (Pyridazines); 0 (Pyrimidines); 0 (Receptor, Endothelin A); 0 (Receptor, Endothelin B); 0 (Receptors, Vasopressin); 0 (Sulfonamides); 113-79-1 (Arginine Vasopressin); 4964P6T9RB (Aldosterone); HW6NV07QEC (ambrisentan); Q326023R30 (bosentan); Z9K9Y9WMVL (macitentan)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170424
[Lr] Data última revisão:
170424
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.116.234930


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[PMID]:28116771
[Au] Autor:Hennenberg M; Acevedo A; Wiemer N; Kan A; Tamalunas A; Wang Y; Yu Q; Rutz B; Ciotkowska A; Herlemann A; Strittmatter F; Stief CG; Gratzke C
[Ad] Endereço:Department of Urology, Ludwig-Maximilians University, Munich, Germany.
[Ti] Título:Non-Adrenergic, Tamsulosin-Insensitive Smooth Muscle Contraction is Sufficient to Replace α -Adrenergic Tension in the Human Prostate.
[So] Source:Prostate;77(7):697-707, 2017 May.
[Is] ISSN:1097-0045
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Lower urinary tract symptoms (LUTS) suggestive of benign prostatic hyperplasia may be caused by prostate smooth muscle contraction. Although α -blockers may improve symptoms by prostate smooth muscle relaxation, their efficacy is limited. This may be explained by non-adrenergic mediators causing contraction in parallel to α -adrenoceptors. However, little is known about the relevance and cooperative actions of non-adrenergic mediators in the prostate. METHODS: Prostate tissues were obtained from radical prostatectomy (n = 127 patients). Contractile responses were studied in an organ bath. RESULTS: Endothelin-1 and noradrenaline induced contractions of similar magnitude (116 ± 23 and 117 ± 18% of KCl-induced contractions). Endothelin-2- and -3-induced maximum contractions of 63 ± 8.6 and 71 ± 19% of KCl, while contractions by the thromboxane analog U46619 amounted up to 63 ± 9.4%. Dopamine-induced contractions averaged to 22 ± 4.5% of KCl, while maximum contractions by serotonin, histamine, and carbachol stayed below 10% of KCl-induced. While noradrenaline-induced contractions were inhibited by tamsulosin (300 nM), endothelin-1-, -2-, or -3-induced contraction were not. No additive effects were observed if endothelins and noradrenaline were applied consecutively to the same samples. If endothelin-1 was applied after U46619, resulting tension (172 ± 43% of KCl) significantly exceeded noradrenaline-induced contraction. Tensions following combined application of endothelin-2 or -3 with U46619 stayed below noradrenaline-induced contractions. Tension following combined application of all three endothelins with U46619 resembled maximum noradrenaline-induced tone. CONCLUSIONS: Contractions following concomitant confrontation of human prostate tissue with noradrenaline and endothelin-1 are not additive. Endothelin-1 is sufficient to induce a smooth muscle tone resembling that of noradrenaline. This may replace lacking α -adrenergic tone under therapy with α -blockers, explaining the limited efficacy of α -blockers in LUTS treatment. Contractions by thromboxane and endothelin-1 may be additive, and may exceed α -adrenergic tone. Prostate 77:697-707, 2017. © 2017 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Ácido 15-Hidroxi-11 alfa,9 alfa-(epoximetano)prosta-5,13-dienoico/farmacologia
Músculo Liso
Próstata
Hiperplasia Prostática
Sulfonamidas/farmacologia
[Mh] Termos MeSH secundário: Antagonistas de Receptores Adrenérgicos alfa 1/farmacologia
Células Cultivadas
Endotelinas/metabolismo
Seres Humanos
Masculino
Contração Muscular/efeitos dos fármacos
Contração Muscular/fisiologia
Relaxamento Muscular/efeitos dos fármacos
Relaxamento Muscular/fisiologia
Músculo Liso/metabolismo
Músculo Liso/fisiopatologia
Norepinefrina/metabolismo
Próstata/metabolismo
Próstata/patologia
Hiperplasia Prostática/metabolismo
Hiperplasia Prostática/patologia
Hiperplasia Prostática/fisiopatologia
Estatística como Assunto
Vasoconstritores/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-1 Receptor Antagonists); 0 (Endothelins); 0 (Sulfonamides); 0 (Vasoconstrictor Agents); 76898-47-0 (15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid); G3P28OML5I (tamsulosin); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170720
[Lr] Data última revisão:
170720
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170125
[St] Status:MEDLINE
[do] DOI:10.1002/pros.23293


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[PMID]:28004949
[Au] Autor:Déziel RA; Tasker RA
[Ad] Endereço:Department of Biomedical Sciences.
[Ti] Título:Effects of endothelin-induced prefrontal cortical lesions on delay discounting in the rat.
[So] Source:Behav Neurosci;131(1):11-19, 2017 Feb.
[Is] ISSN:1939-0084
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Stroke is one of the most prominent causes of neurological disability, and the number of stroke cases worldwide is expected to grow due to increases in both average life span and population. As such, new methods for both acute treatment and poststroke rehabilitation will be increasingly necessary. Although a number of approaches to restoring motor function poststroke are in development, there are few methods to alleviate the cognitive deficits caused by this disease. As well, there are very few preclinical models of stroke with a specific focus on higher-order cognitive functions. The goal of the current experiments was to examine the effects of bilateral ischemic lesions, produced by targeted microinjections of endothelin-1 (ET-1) in the medial (mPFC) and orbital (oPFC) prefrontal cortices of adult male Sprague-Dawley rats (n = 39) on inhibitory control as measured through a delay discounting paradigm. The ET-1 injections to the mPFC and oPFC resulted in average lesion volumes of 17.98 mm3 ± 2.841 mm3 (Mean ± SE) and 26.05 mm3 ± 4.052 mm3 (Mean ± SE), respectively. During delay discounting testing, wherein animals were offered a small, immediately available food reward versus a large, but delayed reward, it was found that animals with lesions to the oPFC were more likely to choose the immediately available reward as compared to their mPFC or control counterparts. We conclude that using ET-1 in the oPFC may be a new and viable method to study the effects of ischemic lesions on higher-order cognitive dysfunction poststroke. (PsycINFO Database Record
[Mh] Termos MeSH primário: Desvalorização pelo Atraso/fisiologia
Córtex Pré-Frontal/fisiologia
Acidente Vascular Cerebral/fisiopatologia
Acidente Vascular Cerebral/psicologia
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/induzido quimicamente
Isquemia Encefálica/fisiopatologia
Isquemia Encefálica/psicologia
Desvalorização pelo Atraso/efeitos dos fármacos
Endotelinas/administração & dosagem
Função Executiva/efeitos dos fármacos
Função Executiva/fisiologia
Inibição (Psicologia)
Masculino
Córtex Pré-Frontal/efeitos dos fármacos
Ratos
Ratos Sprague-Dawley
Recompensa
Acidente Vascular Cerebral/induzido quimicamente
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161223
[St] Status:MEDLINE
[do] DOI:10.1037/bne0000179



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