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Pesquisa : D27.505.519.364.500 [Categoria DeCS]
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[PMID]:29267497
[Au] Autor:Caires A; Fernandes GS; Leme AM; Castino B; Pessoa EA; Fernandes SM; Fonseca CD; Vattimo MF; Schor N; Borges FT
[Ad] Endereço:Disciplina de Nefrologia, Departamento de Medicina, Universidade Federal de São Paulo, São Paulo, SP, Brasil.
[Ti] Título:Endothelin-1 receptor antagonists protect the kidney against the nephrotoxicity induced by cyclosporine-A in normotensive and hypertensive rats.
[So] Source:Braz J Med Biol Res;51(2):e6373, 2017 Dec 11.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Cyclosporin-A (CsA) is an immunosuppressant associated with acute kidney injury and chronic kidney disease. Nephrotoxicity associated with CsA involves the increase in afferent and efferent arteriole resistance, decreased renal blood flow (RBF) and glomerular filtration. The aim of this study was to evaluate the effect of Endothelin-1 (ET-1) receptor blockade with bosentan (BOS) and macitentan (MAC) antagonists on altered renal function induced by CsA in normotensive and hypertensive animals. Wistar and genetically hypertensive rats (SHR) were separated into control group, CsA group that received intraperitoneal injections of CsA (40 mg/kg) for 15 days, CsA+BOS and CsA+MAC that received CsA and BOS (5 mg/kg) or MAC (25 mg/kg) by gavage for 15 days. Plasma creatinine and urea, mean arterial pressure (MAP), RBF and renal vascular resistance (RVR), and immunohistochemistry for ET-1 in the kidney cortex were measured. CsA decreased renal function, as shown by increased creatinine and urea. There was a decrease in RBF and an increase in MAP and RVR in normotensive and hypertensive animals. These effects were partially reversed by ET-1 antagonists, especially in SHR where increased ET-1 production was observed in the kidney. Most MAC effects were similar to BOS, but BOS seemed to be better at reversing cyclosporine-induced changes in renal function in hypertensive animals. The results of this work suggested the direct participation of ET-1 in renal hemodynamics changes induced by cyclosporin in normotensive and hypertensive rats. The antagonists of ET-1 MAC and BOS reversed part of these effects.
[Mh] Termos MeSH primário: Lesão Renal Aguda/induzido quimicamente
Lesão Renal Aguda/prevenção & controle
Ciclosporina/toxicidade
Antagonistas do Receptor de Endotelina A/farmacologia
Imunossupressores/toxicidade
Pirimidinas/farmacologia
Sulfonamidas/farmacologia
[Mh] Termos MeSH secundário: Lesão Renal Aguda/fisiopatologia
Animais
Creatinina/sangue
Antagonistas do Receptor de Endotelina A/uso terapêutico
Hemodinâmica
Immunoblotting
Imuno-Histoquímica
Rim/efeitos dos fármacos
Rim/fisiopatologia
Masculino
Estresse Oxidativo/fisiologia
Substâncias Protetoras/farmacologia
Substâncias Protetoras/uso terapêutico
Pirimidinas/uso terapêutico
Ratos Endogâmicos SHR
Ratos Wistar
Reprodutibilidade dos Testes
Sulfonamidas/uso terapêutico
Resultado do Tratamento
Ureia/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin A Receptor Antagonists); 0 (Immunosuppressive Agents); 0 (Protective Agents); 0 (Pyrimidines); 0 (Sulfonamides); 83HN0GTJ6D (Cyclosporine); 8W8T17847W (Urea); AYI8EX34EU (Creatinine); Q326023R30 (bosentan); Z9K9Y9WMVL (macitentan)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE


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[PMID]:28463833
[Au] Autor:Fujimura M; Joo JY; Kim JS; Hatta M; Yokoyama Y; Tominaga T
[Ad] Endereço:Department of Neurosurgery, Tohoku University Graduate School of Medicine, Sendai, Japan.
[Ti] Título:Preventive Effect of Clazosentan against Cerebral Vasospasm after Clipping Surgery for Aneurysmal Subarachnoid Hemorrhage in Japanese and Korean Patients.
[So] Source:Cerebrovasc Dis;44(1-2):59-67, 2017.
[Is] ISSN:1421-9786
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Clazosentan has been explored worldwide for the prophylaxis of cerebral vasospasm after aneurysmal subarachnoid hemorrhage (aSAH). In a dose-finding trial (CONSCIOUS-1) conducted in Israel, Europe, and North America, clazosentan (1, 5, and 15 mg/h) significantly reduced the incidence of cerebral vasospasm, but its efficacy in Japanese and Korean patients was unknown. We conducted a double-blind comparative study to evaluate the occurrence of cerebral vasospasm in Japanese and Korean patients with aSAH. METHODS: The aim of this multicenter, double-blind, randomized, placebo-controlled, dose-finding phase 2 clinical trial, was to evaluate the efficacy, pharmacokinetics, and safety of clazosentan (5 and 10 mg/h) against cerebral vasospasm after clipping surgery in Japanese and Korean patients with aSAH. Patients aged between 20 and 75 years were administered the study drug within 56 h after the aneurysm rupture and up to day 14 post-aSAH. The incidence of vasospasm, defined as an inner artery diameter reduction of major intracranial arteries ≥34% based on catheter angiography, was compared between each treatment group. Cerebral infarction due to vasospasm at 6 weeks and patients' outcome at 3 months was also compared. RESULTS: Among 181 enrolled patients, 158 completed the study and were analyzed. The incidence of vasospasm up to day 14 after aSAH onset was 80.0% in the placebo group (95% CI 67.0-89.6), 38.5% in the 5 mg/h clazosentan group (95% CI 25.3-53.0), and 35.3% in the 10 mg/h clazosentan group (95% CI 22.4-49.9), indicating that the incidence of vasospasm was significantly reduced by clazosentan treatment (placebo vs. 5 mg/h clazosentan, p < 0.0001; placebo vs. 10 mg/h clazosentan, p < 0.0001). The occurrence of cerebral infarction due to vasospasm was 20.8% in the placebo group (95% CI 10.8-34.1), 3.8% in the 5 mg/h clazosentan group (95% CI 0.5-13.2), and 4.2% in the 10 mg/h clazosentan group (95% CI 0.5-14.3), indicating that clazosentan significantly reduced the occurrence of cerebral infarctions caused by vasospasm (placebo vs. 5 mg/h clazosentan, p = 0.0151; placebo vs. 10 mg/h clazosentan, p = 0.0165). The overall incidence of all-cause death and/or vasospasm-related morbidity/mortality was significantly reduced in the 10 mg/h clazosentan group compared with the placebo group (p = 0.0003). CONCLUSION: These results suggest that clazosentan prevents cerebral vasospasm and subsequent cerebral infarction, and could thereby improve outcomes after performing a clipping surgery for aSAH in Japanese and Korean patients.
[Mh] Termos MeSH primário: Infarto Cerebral/prevenção & controle
Dioxanos/uso terapêutico
Antagonistas do Receptor de Endotelina A/uso terapêutico
Procedimentos Neurocirúrgicos/efeitos adversos
Piridinas/uso terapêutico
Pirimidinas/uso terapêutico
Hemorragia Subaracnóidea/cirurgia
Sulfonamidas/uso terapêutico
Tetrazóis/uso terapêutico
Vasodilatadores/uso terapêutico
Vasoespasmo Intracraniano/prevenção & controle
[Mh] Termos MeSH secundário: Adulto
Idoso
Angiografia Digital
Angiografia Cerebral/métodos
Infarto Cerebral/diagnóstico por imagem
Infarto Cerebral/etiologia
Infarto Cerebral/fisiopatologia
Dioxanos/efeitos adversos
Dioxanos/farmacocinética
Método Duplo-Cego
Antagonistas do Receptor de Endotelina A/efeitos adversos
Antagonistas do Receptor de Endotelina A/farmacocinética
Feminino
Seres Humanos
Japão
Masculino
Meia-Idade
Piridinas/efeitos adversos
Piridinas/farmacocinética
Pirimidinas/efeitos adversos
Pirimidinas/farmacocinética
República da Coreia
Hemorragia Subaracnóidea/diagnóstico por imagem
Hemorragia Subaracnóidea/fisiopatologia
Sulfonamidas/efeitos adversos
Sulfonamidas/farmacocinética
Tetrazóis/efeitos adversos
Tetrazóis/farmacocinética
Fatores de Tempo
Resultado do Tratamento
Vasodilatadores/efeitos adversos
Vasodilatadores/farmacocinética
Vasoespasmo Intracraniano/diagnóstico por imagem
Vasoespasmo Intracraniano/etiologia
Vasoespasmo Intracraniano/fisiopatologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Dioxanes); 0 (Endothelin A Receptor Antagonists); 0 (Pyridines); 0 (Pyrimidines); 0 (Sulfonamides); 0 (Tetrazoles); 0 (Vasodilator Agents); 3DRR0X4728 (clazosentan)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1159/000475824


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[PMID]:28720331
[Au] Autor:Park BG; Shin WS; Oh S; Park GM; Kim NI; Lee S
[Ad] Endereço:Department of Physiology, Catholic Kwandong University College of Medicine, Gangneung 25601, Republic of Korea; Institute for Clinical and Translational Research, Catholic Kwandong University College of Medicine, Gangneung 25601, Republic of Korea.
[Ti] Título:A novel antihypertension agent, sargachromenol D from marine brown algae, Sargassum siliquastrum, exerts dual action as an L-type Ca channel blocker and endothelin A/B receptor antagonist.
[So] Source:Bioorg Med Chem;25(17):4649-4655, 2017 Sep 01.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:We isolated the novel vasoactive marine natural products, (5E,10E)-14-hydroxy-2,6,10-trimethylpentadeca-5,10-dien-4-one (4) and sargachromenol D (5), from Sargassum siliquastrum collected from the coast of the East Sea in South Korea by using activity-guided HPLC purification. The compounds effectively dilated depolarization (50mMK )-induced basilar artery contraction with EC values of 3.52±0.42 and 1.62±0.63µM, respectively, but only sargachromenol D (5) showed a vasodilatory effect on endothelin-1 (ET-1)-induced basilar artery contraction (EC =9.8±0.6µM). These results indicated that sargachromenol D (5) could act as a dual antagonist of l-type Ca channel and endothelin A/B receptors. Moreover, sargachromenol D (5) lowered blood pressure in spontaneous hypertensive rats (SHRs) 2h after oral treatment at a dose of 80mg/kg dose and the effect was maintained for 24h. Based on our ex vivo and in vivo experiments, we propose that sargachromenol D (5) is a strong candidate for the treatment of hypertension that is not controlled by conventional drugs, in particular, severe-, type II diabetes-, salt-sensitive, and metabolic disease-induced hypertension.
[Mh] Termos MeSH primário: Anti-Hipertensivos/química
Benzopiranos/química
Bloqueadores dos Canais de Cálcio/química
Antagonistas do Receptor de Endotelina A/química
Antagonistas do Receptor de Endotelina B/química
Feófitas/química
[Mh] Termos MeSH secundário: Administração Oral
Animais
Anti-Hipertensivos/isolamento & purificação
Anti-Hipertensivos/farmacologia
Artéria Basilar/efeitos dos fármacos
Artéria Basilar/fisiologia
Benzopiranos/isolamento & purificação
Benzopiranos/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Bloqueadores dos Canais de Cálcio/isolamento & purificação
Bloqueadores dos Canais de Cálcio/farmacologia
Canais de Cálcio Tipo L/química
Canais de Cálcio Tipo L/metabolismo
Antagonistas do Receptor de Endotelina A/isolamento & purificação
Antagonistas do Receptor de Endotelina A/farmacologia
Antagonistas do Receptor de Endotelina B/isolamento & purificação
Antagonistas do Receptor de Endotelina B/farmacologia
Masculino
Feófitas/metabolismo
Coelhos
Ratos
Ratos Endogâmicos SHR
Receptor de Endotelina A/química
Receptor de Endotelina A/metabolismo
Receptor de Endotelina B/química
Receptor de Endotelina B/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Benzopyrans); 0 (Calcium Channel Blockers); 0 (Calcium Channels, L-Type); 0 (Endothelin A Receptor Antagonists); 0 (Endothelin B Receptor Antagonists); 0 (Receptor, Endothelin A); 0 (Receptor, Endothelin B); 0 (sargachromenol)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170720
[St] Status:MEDLINE


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[PMID]:28597546
[Au] Autor:Russignan A; Spina C; Tamassia N; Cassaro A; Rigo A; Bagnato A; Rosanò L; Bonalumi A; Gottardi M; Zanatta L; Giacomazzi A; Scupoli MT; Tinelli M; Salvadori U; Mosna F; Zamò A; Cassatella MA; Vinante F; Tecchio C
[Ad] Endereço:Haematology and Bone-Marrow Transplant Unit, Department of Medicine, Verona University, Verona, Italy.
[Ti] Título:Endothelin-1 receptor blockade as new possible therapeutic approach in multiple myeloma.
[So] Source:Br J Haematol;178(5):781-793, 2017 Sep.
[Is] ISSN:1365-2141
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:New effective treatments are needed to improve outcomes for multiple myeloma (MM) patients. Receptors with restricted expression on plasma cells (PCs) represent attractive new therapeutic targets. The endothelin-1 (EDN1) axis, consisting of EDN1 acting through EDN-receptor A (EDNRA) and B (EDNRB), was previously shown to be overexpressed in several tumours, including MM. However, there is incomplete understanding of how EDN1 axis regulates MM growth and response to therapy. Besides EDNRA, the majority of MM cell lines and primary malignant PCs express high levels of EDNRB and release EDN1. Similarly, bone-marrow microenvironment cells also secrete EDN1. Investigating the extent of epigenetic dysregulation of EDNRB gene in MM, we found that hypermethylation of EDNRB promoter and subsequent down-regulation of EDNRB gene was observed in PCs or B lymphocytes from healthy donors compared to EDNRB-expressing malignant PCs. Pharmacological blockade with the dual EDN1 receptor antagonist bosentan decreased cell viability and MAPK activation of U266 and RPMI-8226 cells. Interestingly, the combination of bosentan and the proteasome inhibitor bortezomib, currently approved for MM treatment, resulted in synergistic cytotoxic effects. Overall, our data has uncovered EDN1-mediated autocrine and paracrine mechanisms that regulate malignant PCs growth and drug response, and support EDN1 receptors as new therapeutic targets in MM.
[Mh] Termos MeSH primário: Antagonistas do Receptor de Endotelina A/farmacologia
Mieloma Múltiplo/sangue
Receptor de Endotelina A/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Comunicação Autócrina/fisiologia
Bortezomib/farmacologia
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Sobrevivência Celular/fisiologia
Metilação de DNA
DNA de Neoplasias/genética
Sinergismo Farmacológico
Endotelina-1/sangue
Endotelina-1/fisiologia
Feminino
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Masculino
Meia-Idade
Terapia de Alvo Molecular/métodos
Mieloma Múltiplo/genética
Mieloma Múltiplo/patologia
Plasmócitos/metabolismo
Regiões Promotoras Genéticas
Receptor de Endotelina A/genética
Sulfonamidas/farmacologia
Células Tumorais Cultivadas/efeitos dos fármacos
Células Tumorais Cultivadas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Neoplasm); 0 (Endothelin A Receptor Antagonists); 0 (Endothelin-1); 0 (Receptor, Endothelin A); 0 (Sulfonamides); 69G8BD63PP (Bortezomib); Q326023R30 (bosentan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE
[do] DOI:10.1111/bjh.14771


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[PMID]:28348063
[Au] Autor:Kasztan M; Fox BM; Speed JS; De Miguel C; Gohar EY; Townes TM; Kutlar A; Pollock JS; Pollock DM
[Ad] Endereço:Cardio-Renal Physiology and Medicine, Department of Medicine, and.
[Ti] Título:Long-Term Endothelin-A Receptor Antagonism Provides Robust Renal Protection in Humanized Sickle Cell Disease Mice.
[So] Source:J Am Soc Nephrol;28(8):2443-2458, 2017 Aug.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sickle cell disease (SCD)-associated nephropathy is a major source of morbidity and mortality in patients because of the lack of efficacious treatments targeting renal manifestations of the disease. Here, we describe a long-term treatment strategy with the selective endothelin-A receptor (ET ) antagonist, ambrisentan, designed to interfere with the development of nephropathy in a humanized mouse model of SCD. Ambrisentan preserved GFR at the level of nondisease controls and prevented the development of proteinuria, albuminuria, and nephrinuria. Microscopy studies demonstrated prevention of podocyte loss and structural alterations, the absence of vascular congestion, and attenuation of glomerulosclerosis in treated mice. Studies in isolated glomeruli showed that treatment reduced inflammation and oxidative stress. At the level of renal tubules, ambrisentan treatment prevented the increased excretion of urinary tubular injury biomarkers. Additionally, the treatment strategy prevented tubular brush border loss, diminished tubular iron deposition, blocked the development of interstitial fibrosis, and prevented immune cell infiltration. Furthermore, the prevention of albuminuria in treated mice was associated with preservation of cortical megalin expression. In a separate series of identical experiments, combined ET and ET receptor antagonism provided only some of the protection observed with ambrisentan, highlighting the importance of exclusively targeting the ET receptor in SCD. Our results demonstrate that ambrisentan treatment provides robust protection from diverse renal pathologies in SCD mice, and suggest that long-term ET receptor antagonism may provide a strategy for the prevention of renal complications of SCD.
[Mh] Termos MeSH primário: Anemia Falciforme/complicações
Antagonistas do Receptor de Endotelina A/uso terapêutico
Nefropatias/etiologia
Nefropatias/prevenção & controle
Fenilpropionatos/uso terapêutico
Piridazinas/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Feminino
Seres Humanos
Masculino
Camundongos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin A Receptor Antagonists); 0 (Phenylpropionates); 0 (Pyridazines); HW6NV07QEC (ambrisentan)
[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:170329
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016070711


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[PMID]:28287881
[Au] Autor:Sedláková L; Certíková Chábová V; Dolezelová S; Skaroupková P; Kopkan L; Husková Z; Cervenková L; Kikerlová S; Vanecková I; Sadowski J; Kompanowska-Jezierska E; Kujal P; Kramer HJ; Cervenka L
[Ad] Endereço:a Center for Experimental Medicine, Institute for Clinical and Experimental Medicine , Prague , Czech Republic.
[Ti] Título:Renin-angiotensin system blockade alone or combined with ET receptor blockade: effects on the course of chronic kidney disease in 5/6 nephrectomized Ren-2 transgenic hypertensive rats.
[So] Source:Clin Exp Hypertens;39(2):183-195, 2017.
[Is] ISSN:1525-6006
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Early addition of endothelin (ET) type A (ET ) receptor blockade to complex renin-angiotensin system (RAS) blockade has previously been shown to provide better renoprotection against progression of chronic kidney disease (CKD) in Ren-2 transgenic hypertensive rats (TGR) after 5/6 renal ablation (5/6 NX). In this study, we examined if additional protection is provided when ET blockade is applied in rats with already developed CKD. METHODS: For complex RAS inhibition, an angiotensin-converting enzyme inhibitor along with angiotensin II type 1 receptor blocker was used. Alternatively, ET receptor blocker was added to the RAS blockade. The treatments were initiated 6 weeks after 5/6 NX and the follow-up period was 50 weeks. RESULTS: When applied in established CKD, addition of ET receptor blockade to the complex RAS blockade brought no further improvement of the survival rate (30% in both groups); surprisingly, aggravated albuminuria (588 ± 47 vs. 245 ± 38 mg/24 h, p < 0.05) did not reduce renal glomerular injury index (1.25 ± 0.29 vs. 1.44 ± 0.26), did not prevent the decrease in creatinine clearance (203 ± 21 vs. 253 ± 17 µl/min/100 g body weight), and did not attenuate cardiac hypertrophy to a greater extent than observed in 5/6 NX TGR treated with complex RAS blockade alone. CONCLUSIONS: When applied in the advanced phase of CKD, addition of ET receptor blockade to the complex RAS blockade brings no further beneficial renoprotective effects on the CKD progression in 5/6 NX TGR, in addition to those seen with RAS blockade alone.
[Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Inibidores da Enzima Conversora de Angiotensina/farmacologia
Pressão Sanguínea/efeitos dos fármacos
Antagonistas do Receptor de Endotelina A/farmacologia
Taxa de Filtração Glomerular/efeitos dos fármacos
Rim/efeitos dos fármacos
Insuficiência Renal Crônica/metabolismo
Sistema Renina-Angiotensina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Albuminúria
Angiotensinas/efeitos dos fármacos
Angiotensinas/metabolismo
Animais
Cardiomegalia
Creatinina/metabolismo
Progressão da Doença
Quimioterapia Combinada
Hipertensão
Indóis/farmacologia
Rim/metabolismo
Losartan/farmacologia
Masculino
Nefrectomia
Pirrolidinas/farmacologia
Ratos
Ratos Sprague-Dawley
Ratos Transgênicos
Receptor de Endotelina A/efeitos dos fármacos
Receptor de Endotelina A/metabolismo
Receptor de Endotelina B/efeitos dos fármacos
Receptor de Endotelina B/metabolismo
Renina/efeitos dos fármacos
Renina/metabolismo
Taxa de Sobrevida
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Angiotensins); 0 (Endothelin A Receptor Antagonists); 0 (Indoles); 0 (Pyrrolidines); 0 (Receptor, Endothelin A); 0 (Receptor, Endothelin B); 1T0N3G9CRC (trandolapril); AYI8EX34EU (Creatinine); EC 3.4.23.15 (Renin); JMS50MPO89 (Losartan); V6D7VK2215 (atrasentan)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170602
[Lr] Data última revisão:
170602
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE
[do] DOI:10.1080/10641963.2016.1235184


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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]:28257550
[Au] Autor:Safdar Z; Thakur A; Frost A
[Ad] Endereço:From the Division of Pulmonary-Critical Care Medicine, Baylor College of Medicine, Houston, Texas.
[Ti] Título:Tolerability of Switch to Macitentan from Bosentan in Pulmonary Arterial Hypertension.
[So] Source:South Med J;110(3):223-228, 2017 Mar.
[Is] ISSN:1541-8243
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Pulmonary arterial hypertension (PAH) is a progressive disease that can be treated with several medications. Macitentan, an endothelin receptor antagonist (ERA), has received approval as a PAH therapy. We report our data regarding the tolerability in patients with PAH who were switched from bosentan to macitentan. METHODS: At the Baylor Pulmonary Hypertension Program, 24 patients with PAH who had been taking bosentan and were switched to macitentan were identified in this retrospective study. Data from these patients who switched from bosentan 125 mg orally twice per day to macitentan 10 mg orally daily (between October 2013 and February 2015) when macitentan became commercially available were collected. Patients were advised to take their last evening dose of bosentan and then take the first dose of macitentan the following morning within 12 to 24 hours of the last bosentan dose. Baseline data and postswitch data, including 6-minute walk distance, brain naturietic peptide, alanine transaminase (ALT) and aspartate transaminase (AST) levels, World Health Organization Functional Class (WHO FC), Borg dyspnea score, presence of peripheral edema. RESULTS: At the time of the switch, the mean age was 58 ± 13 (mean ± standard deviation) years, the duration of disease was 6.6 ± 4.4 years, 21 patients were women, 54% were white, and 25% had idiopathic PAH. The mean duration of follow-up after the switch was 5.7 ± 1.5 months. The 6-minute walk distance was 344 ± 106 m preswitch and 319 ± 85 m postswitch ( = 0.18). Brain naturietic peptide levels were 91 ± 170 pg/mL preswitch and 90 ± 137 pg/mL postswitch ( = 0.93). At the time of the switch, 42% were WHO FC II and 50% had edema, and 55% had edema. AST and ALT remained unchanged postswitch. Two patients did not tolerate the switch to macitentan and had to be returned to bosentan: one patient with portopulmonary hypertension developed elevated AST and ALT and the second patient's macitentan was stopped because of malaise and tachyarrhythmia. One patient who underwent a successful liver transplant had macitentan stopped following the transplant. CONCLUSIONS: A rapid switch from bosentan to macitentan was well tolerated and safe with maintained WHO FC, with no significant change in edema and liver enzyme levels. The switch from bosentan to macitentan eliminates the need for monthly liver function test monitoring and removes the potential for bosentan treatment interruption.
[Mh] Termos MeSH primário: Anti-Hipertensivos/uso terapêutico
Antagonistas do Receptor de Endotelina A/uso terapêutico
Hipertensão Pulmonar/tratamento farmacológico
Pirimidinas/uso terapêutico
Sulfonamidas/uso terapêutico
[Mh] Termos MeSH secundário: Alanina Transaminase/análise
Aspartato Aminotransferases/análise
Edema/etiologia
Feminino
Seres Humanos
Masculino
Meia-Idade
Peptídeo Natriurético Encefálico/análise
Estudos Retrospectivos
Teste de Caminhada
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Endothelin A Receptor Antagonists); 0 (Pyrimidines); 0 (Sulfonamides); 114471-18-0 (Natriuretic Peptide, Brain); EC 2.6.1.1 (Aspartate Aminotransferases); EC 2.6.1.2 (Alanine Transaminase); Q326023R30 (bosentan); Z9K9Y9WMVL (macitentan)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170525
[Lr] Data última revisão:
170525
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170304
[St] Status:MEDLINE
[do] DOI:10.14423/SMJ.0000000000000607


  9 / 945 MEDLINE  
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[PMID]:28216625
[Au] Autor:Baretella O; Chung SK; Xu A; Vanhoutte PM
[Ad] Endereço:Department of Pharmacology & Pharmacy, the University of Hong Kong, Hong Kong SAR, China.
[Ti] Título:Endothelial overexpression of endothelin-1 modulates aortic, carotid, iliac and renal arterial responses in obese mice.
[So] Source:Acta Pharmacol Sin;38(4):498-512, 2017 Apr.
[Is] ISSN:1745-7254
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endothelin-1 (ET-1) is essential for mammalian development and life, but it has also been implicated in increased cardiovascular risk under pathophysiological conditions. The aim of this study was to determine the impact of endothelial overexpression of the prepro-endothelin-1 gene on endothelium-dependent and endothelium-independent responses in the conduit and renal arteries of lean and obese mice. Obesity was induced by high-fat-diet (HFD) consumption in mice with Tie-1 promoter-driven, endothelium-specific overexpression of the prepro-endothelin-1 gene (TET ) and in wild-type (WT) littermates on a C57BL/6N background. Isometric tension was measured in rings (with endothelium) of the aorta (A), carotid (CA) and iliac (IA) arteries as well as the main (MRA) and segmental renal (SRA) arteries; all experiments were conducted in the absence or presence of L-NAME and/or the COX inhibitor meclofenamate. The release of prostacyclin and thromboxane A2 was measured by ELISA. In the MRA, TET per se increased contractions to endothelin-1, but the response was decreased in SRA in response to serotonin; there were also improved relaxations to acetylcholine but not insulin in the SRA in the presence of L-NAME. HFD per se augmented the contractions to endothelin-1 (MRA) and to the thromboxane prostanoid (TP) receptor agonist U46619 (CA, MRA) as well as facilitated relaxations to isoproterenol (A). The combination of HFD and TET overexpression increased the contractions of MRA and SRA to vasoconstrictors but not in the presence of meclofenamate; this combination also augmented further relaxations to isoproterenol in the A. Contractions to endothelin-1 in the IA were prevented by endothelin-A receptor antagonist BQ-123 but only attenuated in obese mice by BQ-788. The COX-1 inhibitor FR122047 abolished the contractions of CA to acetylcholine. The release of prostacyclin during the latter condition was augmented in samples from obese TET mice and abolished by FR122047. These findings suggest that endothelial TET overexpression in lean animals has minimal effects on vascular responsiveness. However, if comorbid with obesity, endothelin-1-modulated, prostanoid-mediated renal arterial dysfunction becomes apparent.
[Mh] Termos MeSH primário: Artérias/metabolismo
Células Endoteliais/metabolismo
Endotelina-1/metabolismo
Obesidade/fisiopatologia
[Mh] Termos MeSH secundário: Acetilcolina/farmacologia
Animais
Aorta/metabolismo
Aorta/fisiopatologia
Artérias/fisiopatologia
Artérias Carótidas/metabolismo
Artérias Carótidas/fisiopatologia
Ciclo-Oxigenase 1
Dieta Hiperlipídica/efeitos adversos
Antagonistas do Receptor de Endotelina A/farmacologia
Artéria Ilíaca/metabolismo
Artéria Ilíaca/fisiopatologia
Masculino
Proteínas de Membrana/antagonistas & inibidores
Camundongos Transgênicos
Contração Muscular
Relaxamento Muscular
Músculo Liso Vascular/fisiopatologia
Óxido Nítrico Sintase/antagonistas & inibidores
Obesidade/etiologia
Obesidade/metabolismo
Receptores de Tromboxanos/metabolismo
Artéria Renal/metabolismo
Artéria Renal/fisiopatologia
Tromboxano A2/metabolismo
Vasoconstritores/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin A Receptor Antagonists); 0 (Endothelin-1); 0 (Membrane Proteins); 0 (Receptors, Thromboxane); 0 (Vasoconstrictor Agents); 57576-52-0 (Thromboxane A2); EC 1.14.13.39 (Nitric Oxide Synthase); EC 1.14.99.1 (Cyclooxygenase 1); EC 1.14.99.1 (Ptgs1 protein, mouse); N9YNS0M02X (Acetylcholine)
[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:170221
[St] Status:MEDLINE
[do] DOI:10.1038/aps.2016.138


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[PMID]:28174289
[Au] Autor:Schinzari F; Veneziani A; Mores N; Barini A; Di Daniele N; Cardillo C; Tesauro M
[Ad] Endereço:Department of Internal Medicine, Catholic University, Rome, Italy.
[Ti] Título:Vascular Effects of Obestatin in Lean and Obese Subjects.
[So] Source:Diabetes;66(5):1214-1221, 2017 May.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Obese patients have impaired vasodilator reactivity and increased endothelin 1 (ET-1)-mediated vasoconstriction, two abnormalities contributing to vascular dysfunction. Obestatin, a product of the ghrelin gene, in addition to favorable effects on glucose and lipid metabolism, has shown nitric oxide (NO)-dependent vasodilator properties in experimental models. Given these premises, we compared the effects of exogenous obestatin on forearm flow in lean and obese subjects and assessed its influence on ET-1-dependent vasoconstrictor tone in obesity. In both lean and obese participants, infusion of escalating doses of obestatin resulted in a progressive increase in blood flow from baseline (both < 0.001). This vasodilation was predominantly mediated by enhanced NO activity, because -monomethyl-l-arginine markedly blunted the flow response to obestatin in both groups (both < 0.05 vs. saline). In obese subjects, antagonism of ET receptors by BQ-123 increased forearm flow during saline ( < 0.001) but did not induce additional vasodilation ( > 0.05) during obestatin. Circulating obestatin levels were not different between lean and obese participants ( = 0.41). Our findings indicate that obestatin causes NO-dependent vasodilation in the human circulation. This effect is preserved in obesity, where it is accompanied by reduced ET-1-mediated vasoconstriction. These latter observations make obestatin a promising target for vascular prevention in obesity and diabetes.
[Mh] Termos MeSH primário: Endotélio Vascular/efeitos dos fármacos
Grelina/farmacologia
Obesidade Abdominal
Fluxo Sanguíneo Regional/efeitos dos fármacos
Vasoconstrição/efeitos dos fármacos
Vasodilatação/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Antagonistas do Receptor de Endotelina A/farmacologia
Endotelina-1
Inibidores Enzimáticos/farmacologia
Feminino
Antebraço/irrigação sanguínea
Seres Humanos
Masculino
Óxido Nítrico/metabolismo
Peptídeos Cíclicos/farmacologia
ômega-N-Metilarginina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin A Receptor Antagonists); 0 (Endothelin-1); 0 (Enzyme Inhibitors); 0 (Ghrelin); 0 (Peptides, Cyclic); 27JT06E6GR (omega-N-Methylarginine); 31C4KY9ESH (Nitric Oxide); S2A8YZM151 (cyclo(Trp-Asp-Pro-Val-Leu))
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1067



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