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[PMID]:28449795
[Au] Autor:Packer M; McMurray JJV; Krum H; Kiowski W; Massie BM; Caspi A; Pratt CM; Petrie MC; DeMets D; Kobrin I; Roux S; Swedberg K; ENABLE Investigators and Committees
[Ad] Endereço:Baylor Heart and Vascular Institute, Baylor University Medical Center, Dallas, Texas. Electronic address: milton.packer1526@baylorhealth.edu.
[Ti] Título:Long-Term Effect of Endothelin Receptor Antagonism With Bosentan on the Morbidity and Mortality of Patients With Severe Chronic Heart Failure: Primary Results of the ENABLE Trials.
[So] Source:JACC Heart Fail;5(5):317-326, 2017 May.
[Is] ISSN:2213-1787
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: The objective of this clinical trial was to evaluate the long-term effect of endothelin receptor antagonism with bosentan on the morbidity and mortality of patients with severe chronic heart failure. BACKGROUND: Endothelin may play a role in heart failure, but short-term clinical trials with endothelin receptor antagonists have reported disappointing results. Long-term trials are lacking. METHODS: In 2 identical double-blind trials, we randomly assigned 1,613 patients with New York Heart Association functional class IIIb to IV heart failure and an ejection fraction <35% to receive placebo or bosentan (target dose 125 mg twice daily) for a median of 1.5 years. The primary outcome for each trial was clinical status at 9 months (assessed by the hierarchical clinical composite); the primary outcome across the 2 trials was death from any cause or hospitalization for heart failure. RESULTS: Bosentan did not influence clinical status at 9 months in either trial (p = 0.928 and p = 0.263). In addition, 321 patients in the placebo group and 312 patients in the bosentan group died or were hospitalized for heart failure (hazard ratio [HR]: 1.01; 95% confidence interval [CI]: 0.86 to 1.18; p = 0.90). The bosentan group experienced fluid retention within the first 2 to 4 weeks, as evidenced by increased peripheral edema, weight gain, decreases in hemoglobin, and an increased risk of hospitalization for heart failure, despite intensification of background diuretics. During follow-up, 173 patients died in the placebo group and 160 patients died in the bosentan group (HR: 0.94; 95% CI: 0.75 to 1.16). About 10% of the bosentan group showed meaningful increases in hepatic transaminases, but none had acute or chronic liver failure. CONCLUSIONS: Bosentan did not improve the clinical course or natural history of patients with severe chronic heart failure and but caused early and important fluid retention.
[Mh] Termos MeSH primário: Causas de Morte
Antagonistas dos Receptores de Endotelina/administração & dosagem
Insuficiência Cardíaca/tratamento farmacológico
Sulfonamidas/administração & dosagem
[Mh] Termos MeSH secundário: Idoso
Austrália
Doença Crônica
Relação Dose-Resposta a Droga
Método Duplo-Cego
Esquema de Medicação
Antagonistas dos Receptores de Endotelina/efeitos adversos
Europa (Continente)
Feminino
Insuficiência Cardíaca/diagnóstico
Insuficiência Cardíaca/mortalidade
Seres Humanos
Internacionalidade
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Morbidade
América do Norte
Prognóstico
Modelos de Riscos Proporcionais
Ensaios Clínicos Controlados Aleatórios como Assunto
Medição de Risco
Índice de Gravidade de Doença
Sulfonamidas/efeitos adversos
Análise de Sobrevida
Fatores de Tempo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Endothelin Receptor Antagonists); 0 (Sulfonamides); Q326023R30 (bosentan)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


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[PMID]:28468962
[Au] Autor:Gohar EY; Kasztan M; Becker BK; Speed JS; Pollock DM
[Ad] Endereço:Cardio-Renal Physiology & Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama.
[Ti] Título:Ovariectomy uncovers purinergic receptor activation of endothelin-dependent natriuresis.
[So] Source:Am J Physiol Renal Physiol;313(2):F361-F369, 2017 Aug 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We recently reported that natriuresis produced by renal medullary salt loading is dependent on endothelin (ET)-1 and purinergic (P2) receptors in male rats. Because sex differences in ET-1 and P2 signaling have been reported, we decided to test whether ovarian sex hormones regulate renal medullary ET-1 and P2-dependent natriuresis. The effect of medullary NaCl loading on Na excretion was determined in intact and ovariectomized (OVX) female Sprague-Dawley rats with and without ET-1 or P2 receptor antagonism. Isosmotic saline (284 mosmol/kgH O) was infused in the renal medullary interstitium of anesthetized rats during a baseline urine collection period, followed by isosmotic or hyperosmotic saline (1,800 mosmol/kgH O) infusion. Medullary NaCl loading significantly enhanced Na excretion in intact and OVX female rats. ET or P2 receptor blockade did not attenuate the natriuretic effect of medullary NaCl loading in intact females, whereas ET or P2 receptor blockade attenuated the natriuretic response to NaCl loading in OVX rats. Activation of medullary P2Y and P2Y receptors by UTP infusion had no significant effect in intact females but enhanced Na excretion in OVX rats. Combined ET receptor blockade significantly inhibited the natriuretic response to UTP observed in OVX rats. These data demonstrate that medullary NaCl loading induces ET-1 and P2-independent natriuresis in intact females. In OVX, activation of medullary P2 receptors promotes ET-dependent natriuresis, suggesting that ovarian hormones may regulate the interplay between the renal ET-1 and P2 signaling systems to facilitate Na excretion.
[Mh] Termos MeSH primário: Endotelina-1/metabolismo
Medula Renal/metabolismo
Natriurese
Ovariectomia
Receptores Purinérgicos P2Y2/metabolismo
Receptores Purinérgicos P2/metabolismo
Eliminação Renal
Sódio/urina
[Mh] Termos MeSH secundário: Animais
Antagonistas dos Receptores de Endotelina/farmacologia
Endotelina-1/genética
Feminino
Medula Renal/efeitos dos fármacos
Natriurese/efeitos dos fármacos
Agonistas do Receptor Purinérgico P2/farmacologia
Antagonistas do Receptor Purinérgico P2/farmacologia
Ratos Sprague-Dawley
Receptores Purinérgicos P2/efeitos dos fármacos
Receptores Purinérgicos P2Y2/efeitos dos fármacos
Eliminação Renal/efeitos dos fármacos
Transdução de Sinais
Cloreto de Sódio/administração & dosagem
Cloreto de Sódio/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin Receptor Antagonists); 0 (Endothelin-1); 0 (P2ry2 protein, rat); 0 (Purinergic P2 Receptor Agonists); 0 (Purinergic P2 Receptor Antagonists); 0 (Receptors, Purinergic P2); 0 (Receptors, Purinergic P2Y2); 0 (purinoceptor P2Y4); 451W47IQ8X (Sodium Chloride); 9NEZ333N27 (Sodium)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00098.2017


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[PMID]:27771466
[Au] Autor:Marra AM; Benjamin N; Eichstaedt C; Salzano A; Arcopinto M; Gargani L; D Alto M; Argiento P; Falsetti L; Di Giosia P; Isidori AM; Ferrara F; Bossone E; Cittadini A; Grünig E
[Ad] Endereço:IRCCS SDN, Via Gianturco 113, 80143 Naples, Italy. Electronic address: alberto_marra@hotmail.it.
[Ti] Título:Gender-related differences in pulmonary arterial hypertension targeted drugs administration.
[So] Source:Pharmacol Res;114:103-109, 2016 Dec.
[Is] ISSN:1096-1186
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:During the last 15 years, a real "paradigm-shift" occurred, due to the development of PAH-targeted drugs, leading to crucial improvements in symptoms, exercise capacity, hemodynamics and outcome of PAH patients. In order to describe differences regarding epidemiology and therapy in PAH according to gender, we performed a review of the available literature in "PubMed" and "Web of Science" databases. In order to find relevant articles, we combined each of the following the keywords "pulmonary arterial hypertension", "gender", "sex", "men", "woman", "male", "female", "phosphodiesterase inhibitors", "endothelin receptor antagonists", "prostanoids". While there is a substantial agreement among epidemiological studies in reporting an increased prevalence of pulmonary arterial hypertension (PAH) among women, male PAH patients are affected by a higher impairment of the right ventricular function and consequently experience poorer outcomes. With regards to PAH-targeted drug administration, endothelin receptor antagonists (ERAs) and prostacyclin analogues (PC) show better treatment results in female PAH patients, while phosphodiesterase-5 inhibitors (PD5-I) seem to exert a more beneficial effect on male patients. However, to date no clear consensus could be formed by the available literature, which is constituted mainly by retrospective studies. Females with PAH are more prone to develop PAH, while males experience poorer outcomes. Females PAH might benefit more from ERAs and PC, while males seem to have more beneficial effects from PD5-I administration. However, more research is warranted in order to assess the most effective treatment for PAH patients according to gender.
[Mh] Termos MeSH primário: Anti-Hipertensivos/uso terapêutico
Antagonistas dos Receptores de Endotelina/uso terapêutico
Epoprostenol/uso terapêutico
Hipertensão Pulmonar/tratamento farmacológico
Hipertensão Pulmonar/epidemiologia
Inibidores da Fosfodiesterase 5/uso terapêutico
[Mh] Termos MeSH secundário: Anti-Hipertensivos/administração & dosagem
Antagonistas dos Receptores de Endotelina/administração & dosagem
Epoprostenol/administração & dosagem
Epoprostenol/análogos & derivados
Feminino
Seres Humanos
Hipertensão Pulmonar/fisiopatologia
Masculino
Inibidores da Fosfodiesterase 5/administração & dosagem
Fatores Sexuais
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Endothelin Receptor Antagonists); 0 (Phosphodiesterase 5 Inhibitors); DCR9Z582X0 (Epoprostenol)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161107
[St] Status:MEDLINE


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[PMID]:28462837
[Au] Autor:Khadtare N; Stephani R; Korlipara V
[Ad] Endereço:Department of Pharmaceutical Sciences, College of Pharmacy and Health Sciences, St. John's University, Queens, NY 11439, United States.
[Ti] Título:Design, synthesis and evaluation of 1,3,6-trisubstituted-4-oxo-1,4-dihydroquinoline-2-carboxylic acid derivatives as ET receptor selective antagonists using FRET assay.
[So] Source:Bioorg Med Chem Lett;27(11):2281-2285, 2017 06 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The endothelin axis and in particular the two receptor subtypes, ET and ET , are under investigation for the treatment of various diseases such as pulmonary arterial hypertension, fibrosis, renal failure and cancer. Previous work in our lab has shown that 1,3,6-trisubstituted-4-oxo-1,4-dihydroquinoline-2-carboxylic acid derivatives exhibit noteworthy endothelin receptor antagonist activity. A series of analogues with modifications centered around position 6 of the heterocyclic quinolone core and replacement of the aryl carboxylic acid group with an isosteric tetrazole ring was designed and synthesized to further optimize the structure activity relationship. The endothelin receptor antagonist activity was determined by in vitro Förster resonance energy transfer (FRET) using GeneBLAzer® assay technology. The most potent member of this series exhibited ET receptor antagonist activity in the subnanomolar range with an IC value of 0.8nM, and was 1000-fold selective for the ET receptor compared to the ET receptor. Its activity and selectivity profile resembles that of the most recently approved drug, macitentan.
[Mh] Termos MeSH primário: Ácidos Carboxílicos/química
Ácidos Carboxílicos/farmacologia
Quinolinas/química
Quinolinas/farmacologia
Receptor de Endotelina A/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Ácidos Carboxílicos/síntese química
Antagonistas dos Receptores de Endotelina/síntese química
Antagonistas dos Receptores de Endotelina/química
Antagonistas dos Receptores de Endotelina/farmacologia
Transferência Ressonante de Energia de Fluorescência
Seres Humanos
Concentração Inibidora 50
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (1,4-dihydroquinoline); 0 (Carboxylic Acids); 0 (Endothelin Receptor Antagonists); 0 (Quinolines); 0 (Receptor, Endothelin A)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE


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[PMID]:28805809
[Au] Autor:Shihoya W; Nishizawa T; Yamashita K; Inoue A; Hirata K; Kadji FMN; Okuta A; Tani K; Aoki J; Fujiyoshi Y; Doi T; Nureki O
[Ad] Endereço:Department of Basic Medicinal Sciences, Graduate School of Pharmaceutical Sciences, Nagoya University, Nagoya, Japan.
[Ti] Título:X-ray structures of endothelin ET receptor bound to clinical antagonist bosentan and its analog.
[So] Source:Nat Struct Mol Biol;24(9):758-764, 2017 Sep.
[Is] ISSN:1545-9985
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Endothelin receptors (ETRs) have crucial roles in vascular control and are targets for drugs designed to treat circulatory-system diseases and cancer progression. The nonpeptide dual-ETR antagonist bosentan is the first oral drug approved to treat pulmonary arterial hypertension. Here we report crystal structures of human endothelin ET receptor bound to bosentan and to the ET -selective analog K-8794, at 3.6-Å and 2.2-Å resolution, respectively. The K-8794-bound structure reveals the detailed water-mediated hydrogen-bonding network at the transmembrane core, which could account for the weak negative allosteric modulation of ET by Na ions. The bosentan-bound structure reveals detailed interactions with ET , which are probably conserved in the ET receptor. A comparison of the two structures shows unexpected similarity between antagonist and agonist binding. Despite this similarity, bosentan sterically prevents the inward movement of transmembrane helix 6 (TM6), and thus exerts its antagonistic activity. These structural insights will facilitate the rational design of new ETR-targeting drugs.
[Mh] Termos MeSH primário: Antagonistas dos Receptores de Endotelina/química
Antagonistas dos Receptores de Endotelina/metabolismo
Receptor de Endotelina B/química
Receptor de Endotelina B/metabolismo
Sulfonamidas/química
Sulfonamidas/metabolismo
[Mh] Termos MeSH secundário: Cristalografia por Raios X
Seres Humanos
Modelos Moleculares
Ligação Proteica
Conformação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (EDNRB protein, human); 0 (Endothelin Receptor Antagonists); 0 (Receptor, Endothelin B); 0 (Sulfonamides); Q326023R30 (bosentan)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170815
[St] Status:MEDLINE
[do] DOI:10.1038/nsmb.3450


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[PMID]:28791952
[Au] Autor:Jasinska-Stroschein M; Orszulak-Michalak D
[Ad] Endereço:Zaklad Biofarmacji, Katedra Biofarmacji, Wydzial Farmaceutyczny Uniwersytetu Medycznego w Lodzi.
[Ti] Título:Novel strategies for treatment of pulmonary arterial hypertension.
[So] Source:Postepy Hig Med Dosw (Online);71(0):577-588, 2017 Jul 11.
[Is] ISSN:1732-2693
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Pulmonary hypertension (PH) is a rare disorder associated with abnormally elevated pulmonary pressures that, if untreated, leads to right heart failure and premature death. Special population include patents with pulmonary arterial hypertension (PAH). A greater understanding of the epidemiology, pathogenesis, and pathophysiology of PAH has led to significant advances over the past few years. Modern drug therapy provides a significant improvement in patient symptomatic status and a slower rate of clinical deterioration. Despite this, PAH remains a chronic disease without a cure. There is a need for the development of novel therapies and therapeutic strategies, as treatment options are neither universally available nor always effective, possibly due to the large number of mediator and signaling pathways with downstream effectors which are implicated in the pathobiology of PH, and which are not fully reversed during PAH therapy. In the following pages, we review novel strategies for treatment of PAH. For this purpose we summarized the role of specific drug therapies that involve: endothelin receptor antagonists (ERA), phosphodiesterase type 5 inhibitors (PDE-5i) and prostacyclin and prostanoids (PGI2). We focused on novel molecular mechanisms in PAH of recently approved: Guanylate cyclase stimulator and non-prostanoid IP receptor agonist. We discussed novel approach to combined therapy, as well as a new generation of investigational drugs and promising PAH-associated signaling pathways, such as, PDGF, RhoA/ROCK RAAS, HT-5 and others.
[Mh] Termos MeSH primário: Hipertensão Pulmonar/tratamento farmacológico
[Mh] Termos MeSH secundário: Quimioterapia Combinada
Antagonistas dos Receptores de Endotelina/uso terapêutico
Guanilato Ciclase/efeitos dos fármacos
Seres Humanos
Inibidores da Fosfodiesterase 5/uso terapêutico
Prostaglandinas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Endothelin Receptor Antagonists); 0 (Phosphodiesterase 5 Inhibitors); 0 (Prostaglandins); EC 4.6.1.2 (Guanylate Cyclase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE


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[PMID]:28724039
[Au] Autor:Abuowda Y; Almeida RS; Oliveira AA; Pego P; Santos C; Matos-Costa J
[Ad] Endereço:Clinic of autoimmune diseases, Department of Internal Medicine - III, Hospital Distrital de Santarém, Santarém, Portugal.
[Ti] Título:Treatment of digital ulcers in systemic sclerosis: Case series study of thirteen patients and discussion on outcome.
[So] Source:Rev Assoc Med Bras (1992);63(5):422-426, 2017 May.
[Is] ISSN:1806-9282
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Introduction:: In systemic sclerosis (SSc), digital ulcers (DU) are debilitating and recurrent. They are markers of prognosis and are associated with disability and mortality. Treatment strategies have been developed to block the proposed mechanisms of this complication. Objective:: Clinical description of a population of SSc patients with DU, treatment, complications and outcome. Method:: Analysis of 48 SSc patients meeting 2013 ACR-EULAR criteria, followed between 1999-2015; 13 patients had DU. Treatment protocol applied included cycles of 21 days of alprostadil, which can be repeated in the absence of DU healing. After DU healing, bosentan was initiated. Results:: DU healing was achieved with intravenous prostanoid in 12 patients; seven patients required repeated treatment for DU healing. Twelve patients were later treated with bosentan; three of them experienced recurrence of DU, while one was anti-B2-GPI positive. Four patients had soft tissue loss and three other suffered digital amputation, these being late diagnosis. Conclusion:: Younger patients and early referrals had better outcomes. Endothelin receptor antagonist toxicity should be monitored, particularly in patients previously exposed to hepatotoxic drugs.
[Mh] Termos MeSH primário: Alprostadil/uso terapêutico
Antagonistas dos Receptores de Endotelina/uso terapêutico
Dedos
Escleroderma Sistêmico/complicações
Úlcera Cutânea/tratamento farmacológico
Úlcera Cutânea/etiologia
Sulfonamidas/uso terapêutico
Vasodilatadores/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Relação Dose-Resposta a Droga
Feminino
Dermatoses da Mão/tratamento farmacológico
Dermatoses da Mão/etiologia
Dermatoses da Mão/patologia
Seres Humanos
Masculino
Meia-Idade
Reprodutibilidade dos Testes
Úlcera Cutânea/patologia
Fatores de Tempo
Resultado do Tratamento
Cicatrização/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Endothelin Receptor Antagonists); 0 (Sulfonamides); 0 (Vasodilator Agents); F5TD010360 (Alprostadil); Q326023R30 (bosentan)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170721
[St] Status:MEDLINE


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[PMID]:28640077
[Au] Autor:Omarjee L; Fontaine C; Mahe G; Jaquinandi V
[Ad] Endereço:aUnité de Médecine Vasculaire, INSERM CIC 1414, Pôle Imagerie Médicale et Explorations Fonctionnelles, CHU de Rennes, 35033 Rennes Cedex, France. bMitoVasc Institute, UMR CNRS 6015-INSERM U1083, Angers University Hospital, Angers Cedex cUnité de Médecine Vasculaire, Plateau des Consultations Médicales, Cholet Cedex France.
[Ti] Título:Improvement of peripheral artery disease with Sildenafil and Bosentan combined therapy in a patient with limited cutaneous systemic sclerosis: A case report.
[So] Source:Medicine (Baltimore);96(25):e6988, 2017 Jun.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Sildenafil, a phosphodiesterase-5-inhibitor and Bosentan, an endothelin-1-receptor antagonist combined therapy could have beneficial effect in systemic sclerosis (SSc) patients with peripheral artery disease. PATIENT CONCERNS: We report a case of a 48-year-old Black woman, who developed severe left limb claudication and walking limitation following a left femoropopliteal bypass occlusion in 2014. She was a heavy smoker and had a history of right middle cerebral artery ischemic stroke and bilateral Raynaud phenomenon. DIAGNOSES: According to the American College of Rheumatology/European League Against Rheumatism-2013 criteria, diagnosis of limited cutaneous SSc was retained with macrovascular lesions. She was referred for investigation of left limb claudication on treadmill using transcutaneous oxygen pressure measurement during exercise to argue for the vascular origin of the walking impairment. She had a severe left limb ischemia and the maximum walking distance (MWD) she reached was 118 m in March 2015 despite the medical optimal treatment and walking rehabilitation. INTERVENTIONS: Sildenafil, 20 mg tid, was introduced due to active digital ulcers. In July 2015, the MWD increased to 288 m, then to 452 m in December 2015. Adding Bosentan to Sildenafil to prevent recurrent digital ulcers resulted in an MWD of 1576 m. OUTCOMES: Recently, the patient is treated with the combined therapy. She has no more pain during walking and his quality of life has improved. LESSONS: Sildenafil and Bosentan combined therapy was associated in our case with an improvement of MWD without adverse effect. Further clinical trials are necessary to confirm our original observation.
[Mh] Termos MeSH primário: Fármacos Cardiovasculares/uso terapêutico
Doença Arterial Periférica/complicações
Doença Arterial Periférica/tratamento farmacológico
Escleroderma Sistêmico/complicações
Citrato de Sildenafila/uso terapêutico
Sulfonamidas/uso terapêutico
[Mh] Termos MeSH secundário: Quimioterapia Combinada
Antagonistas dos Receptores de Endotelina/uso terapêutico
Feminino
Seres Humanos
Meia-Idade
Inibidores da Fosfodiesterase 5/uso terapêutico
Escleroderma Sistêmico/tratamento farmacológico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cardiovascular Agents); 0 (Endothelin Receptor Antagonists); 0 (Phosphodiesterase 5 Inhibitors); 0 (Sulfonamides); BW9B0ZE037 (Sildenafil Citrate); Q326023R30 (bosentan)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170623
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000006988


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[PMID]:28606962
[Au] Autor:Planas-Rigol E; Terrades-Garcia N; Corbera-Bellalta M; Lozano E; Alba MA; Segarra M; Espígol-Frigolé G; Prieto-González S; Hernández-Rodríguez J; Preciado S; Lavilla R; Cid MC
[Ad] Endereço:Vasculitis Research Unit, Department of Autoimmune Diseases, Hospital Clinic, University of Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), CRB-CELLEX, Barcelona, Spain.
[Ti] Título:Endothelin-1 promotes vascular smooth muscle cell migration across the artery wall: a mechanism contributing to vascular remodelling and intimal hyperplasia in giant-cell arteritis.
[So] Source:Ann Rheum Dis;76(9):1624-1634, 2017 Sep.
[Is] ISSN:1468-2060
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Giant-cell arteritis (GCA) is an inflammatory disease of large/medium-sized arteries, frequently involving the temporal arteries (TA). Inflammation-induced vascular remodelling leads to vaso-occlusive events. Circulating endothelin-1 (ET-1) is increased in patients with GCA with ischaemic complications suggesting a role for ET-1 in vascular occlusion beyond its vasoactive function. OBJECTIVE: To investigate whether ET-1 induces a migratory myofibroblastic phenotype in human TA-derived vascular smooth muscle cells (VSMC) leading to intimal hyperplasia and vascular occlusion in GCA. METHODS AND RESULTS: Immunofluorescence/confocal microscopy showed increased ET-1 expression in GCA lesions compared with control arteries. In inflamed arteries, ET-1 was predominantly expressed by infiltrating mononuclear cells whereas ET receptors, particularly ET-1 receptor B (ET R), were expressed by both mononuclear cells and VSMC. ET-1 increased TA-derived VSMC migration in vitro and α-smooth muscle actin (αSMA) expression and migration from the media to the intima in cultured TA explants. ET-1 promoted VSMC motility by increasing activation of focal adhesion kinase (FAK), a crucial molecule in the turnover of focal adhesions during cell migration. FAK activation resulted in Y397 autophosphorylation creating binding sites for Src kinases and the p85 subunit of PI3kinases which, upon ET-1 exposure, colocalised with FAK at the focal adhesions of migrating VSMC. Accordingly, FAK or PI3K inhibition abrogated ET-1-induced migration in vitro. Consistently, ET-1 receptor A and ET R antagonists reduced αSMA expression and delayed VSMC outgrowth from cultured GCA-involved artery explants. CONCLUSIONS: ET-1 is upregulated in GCA lesions and, by promoting VSMC migration towards the intimal layer, may contribute to intimal hyperplasia and vascular occlusion in GCA.
[Mh] Termos MeSH primário: Movimento Celular/genética
Endotelina-1/genética
Arterite de Células Gigantes/genética
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
Remodelação Vascular/genética
[Mh] Termos MeSH secundário: Actinas/efeitos dos fármacos
Actinas/genética
Actinas/metabolismo
Idoso
Western Blotting
Estudos de Casos e Controles
Movimento Celular/efeitos dos fármacos
Antagonistas dos Receptores de Endotelina/farmacologia
Endotelina-1/metabolismo
Endotelina-1/farmacologia
Feminino
Imunofluorescência
Quinase 1 de Adesão Focal/antagonistas & inibidores
Quinase 1 de Adesão Focal/metabolismo
Arterite de Células Gigantes/metabolismo
Arterite de Células Gigantes/patologia
Seres Humanos
Hiperplasia
Técnicas In Vitro
Leucócitos Mononucleares
Masculino
Microscopia Confocal
Músculo Liso Vascular/citologia
Miócitos de Músculo Liso/citologia
Miócitos de Músculo Liso/efeitos dos fármacos
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/metabolismo
Fosforilação
Receptor de Endotelina A/efeitos dos fármacos
Receptor de Endotelina A/metabolismo
Receptor de Endotelina B/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Túnica Íntima/patologia
Remodelação Vascular/efeitos dos fármacos
Quinases da Família src/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (Endothelin Receptor Antagonists); 0 (Endothelin-1); 0 (Receptor, Endothelin A); 0 (Receptor, Endothelin B); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.10.2 (Focal Adhesion Kinase 1); EC 2.7.10.2 (PTK2 protein, human); EC 2.7.10.2 (src-Family Kinases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170821
[Lr] Data última revisão:
170821
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE
[do] DOI:10.1136/annrheumdis-2016-210792


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Texto completo
[PMID]:28539568
[Au] Autor:Xiong B; Nie D; Cao Y; Zou Y; Yao Y; Tan J; Qian J; Rong S; Wang C; Huang J
[Ad] Endereço:Department of Cardiology, The Second Affiliated Hospital of Chongqing Medical University.
[Ti] Título:Clinical and Hemodynamic Effects of Endothelin Receptor Antagonists in Patients With Heart Failure.
[So] Source:Int Heart J;58(3):400-408, 2017 May 31.
[Is] ISSN:1349-3299
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The clinical benefit of endothelin receptor antagonists (ERA) for the management of heart failure (HF) remains controversial. To examine this question, we performed a meta-analysis of randomized controlled trials (RCTs) to investigate the clinical and hemodynamic effects of ERA in HF patients.We searched the PubMed, Medline, Embase, and Cochrane Library from inception to March 20, 2016 to identify the pertinent studies. Risk ratio (RR) and weighted mean difference (WMD) were calculated using a fixed or random effect model.A total of 15 RCTs with 3,624 HF patients were included. Compared with control groups, ERA might not improve the mortality (RR 1.12, 95%CI 0.81 to 1.54, P = 0.51) or incidence of worsening HF or cardiovascular events (WHF/ CVE) (RR 1.06, 95%CI 0.94 to 1.19, P = 0.35) in HF patients. Subgroup analysis also suggested that neither nonselective nor selective ERAs had an impact on mortality and WHF/CVE. However, the hemodynamic variables of HF patients, including cardiac index (WMD 0.32, 95%CI 0.22 to 0.43, P < 0.01), pulmonary capillary wedge pressure (WMD -3.10, 95%CI -3.99 to -2.20, P < 0.01), mean pulmonary arterial pressure (WMD -4.42, 95%CI -5.50 to -3.33, P < 0.01), systemic vascular resistance (WMD -276.35, 95%CI -399.62 to -153.09, P < 0.01), and pulmonary vascular resistance (WMD -69.42, 95%CI -105.33 to -33.52, P < 0.01) were significantly improved by ERA.In conclusion, this meta-analysis suggests that ERA therapy could effectively improve cardiac output and pulmonary and systemic hemodynamics, but with less benefit to the clinical outcomes of HF patients.
[Mh] Termos MeSH primário: Antagonistas dos Receptores de Endotelina/uso terapêutico
Insuficiência Cardíaca/tratamento farmacológico
Hemodinâmica/efeitos dos fármacos
[Mh] Termos MeSH secundário: Insuficiência Cardíaca/fisiopatologia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Endothelin Receptor Antagonists)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170809
[Lr] Data última revisão:
170809
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170526
[St] Status:MEDLINE
[do] DOI:10.1536/ihj.16-307



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