Base de dados : MEDLINE
Pesquisa : D27.505.519.162.500 [Categoria DeCS]
Referências encontradas : 8012 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 802 ir para página                         

  1 / 8012 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29286056
[Au] Autor:Zaid Iskandar M; Lang CC
[Ad] Endereço:Ninewells Hospital and Medical School, Dundee, Scotland, UK.
[Ti] Título:Sacubitril and valsartan fixed combination to reduce heart failure events in post-acute myocardial infarction patients.
[So] Source:Drugs Today (Barc);53(10):545-551, 2017 Oct.
[Is] ISSN:1699-3993
[Cp] País de publicação:Spain
[La] Idioma:eng
[Ab] Resumo:Heart failure is a term used to define a constellation of symptoms and signs that are commonly attributed to the inability of the heart to produce a cardiac output that meets the demands of the body. It remains a deadly disease, affecting between 1-2% of the population, and is more common in the elderly, with around 6-10% of patients over 65 suffering from the condition. Sacubitril/valsartan (LCZ-696) is a combined neprilysin inhibitor and angiotensin AT1 receptor blocker approved in recent years for the treatment of chronic heart failure with reduced ejection fraction. In an area where there have been limited pharmacological advances in the last 10 years, this drug was a game changer and a much welcomed addition to contemporary heart failure therapy. It is currently being studied in patients with heart failure with preserved ejection fraction and for the reduction of heart failure events post-acute myocardial infarction. Results from the ongoing PARADISE-MI study are awaited by the global cardiology community with great interest.
[Mh] Termos MeSH primário: Aminobutiratos/administração & dosagem
Bloqueadores do Receptor Tipo 1 de Angiotensina II/administração & dosagem
Insuficiência Cardíaca/tratamento farmacológico
Infarto do Miocárdio/complicações
Neprilisina/antagonistas & inibidores
Tetrazóis/administração & dosagem
Valsartana/administração & dosagem
[Mh] Termos MeSH secundário: Aminobutiratos/farmacologia
Ensaios Clínicos como Assunto
Seres Humanos
Tetrazóis/farmacologia
Valsartana/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (Angiotensin II Type 1 Receptor Blockers); 0 (LCZ 696); 0 (Tetrazoles); 80M03YXJ7I (Valsartan); EC 3.4.24.11 (Neprilysin)
[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:171230
[St] Status:MEDLINE
[do] DOI:10.1358/dot.2017.53.10.2722396


  2 / 8012 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:28471687
[Au] Autor:Certíková Chábová V; Cervenka L
[Ad] Endereço:Department of Nephrology, First Faculty of Medicine, Charles University, Prague, Czech Republic, Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. luce@ikem.cz.
[Ti] Título:The dilemma of dual renin-angiotensin system blockade in chronic kidney disease: why beneficial in animal experiments but not in the clinic?
[So] Source:Physiol Res;66(2):181-192, 2017 May 04.
[Is] ISSN:1802-9973
[Cp] País de publicação:Czech Republic
[La] Idioma:eng
[Ab] Resumo:Drugs interfering with the renin-angiotensin-aldosterone system (RAAS) improved the prognosis in patients with hypertension, heart failure, diabetes and chronic kidney disease. However, combining different drugs brought no further benefit while increasing the risk of hyperkalemia, hypotension and acute renal failure. This was so with combining angiotensin converting enzyme inhibitors (ACEi) and angiotensin II receptors type 1 antagonists (ARB). Dissimilarly, in animal disease models this dual therapy proved clearly superior to single drug treatment and became the optimal standard regime for comparison with other treatments. This review analyzes the causes of the discrepancy of effects of the dual therapy between animal experiments versus clinical studies, and is focused on the outcomes in chronic kidney disease. Discussed is the role of species differences in RAAS, of the variability of the disease features in humans versus relative stability in animals, of the genetic uniformity in the animals but not in humans, and of the biased publication habits of experimental versus clinical studies. We attempt to understand the causes and reconcile the discordant findings and suggest to what extent dual RAAS inhibition should be continued in animal experiments and why its application in the clinics should be limited to strictly selected groups of patients.
[Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/administração & dosagem
Inibidores da Enzima Conversora de Angiotensina/administração & dosagem
Modelos Animais de Doenças
Insuficiência Renal Crônica/tratamento farmacológico
Insuficiência Renal Crônica/imunologia
Sistema Renina-Angiotensina/efeitos dos fármacos
Sistema Renina-Angiotensina/imunologia
[Mh] Termos MeSH secundário: Lesão Renal Aguda/induzido quimicamente
Lesão Renal Aguda/imunologia
Lesão Renal Aguda/prevenção & controle
Inibidores da Enzima Conversora de Angiotensina/efeitos adversos
Animais
Medicina Baseada em Evidências
Seres Humanos
Hiperpotassemia/induzido quimicamente
Hiperpotassemia/imunologia
Hiperpotassemia/prevenção & controle
Hipertensão/induzido quimicamente
Hipertensão/imunologia
Hipertensão/prevenção & controle
Especificidade da Espécie
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Angiotensin-Converting Enzyme Inhibitors)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


  3 / 8012 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29287783
[Au] Autor:da Silva Mansano N; Jorge IF; Chies AB; Viani GA; Spadella MA
[Ad] Endereço:Marília Medical School, Marília, São Paulo, Brazil. Electronic address: maspadella@famema.br.
[Ti] Título:Effects of telmisartan and losartan on irradiated testes.
[So] Source:Life Sci;194:157-167, 2018 Feb 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: To analyze the effects of radiation on the reproductive tissue of male Wistar rats and to evaluate whether treatment with the Ang II AT1 receptor antagonists telmisartan and losartan mitigate the dysfunctions resulting from this exposure. MAIN METHODS: Rats were randomly divided into groups: Control, Irradiated, Telmisartan, Losartan, Irradiated+Telmisartan, and Irradiated+Losartan. Single dose of 5Gy was administered directly into the scrotum, followed by treatment with telmisartan (12mg/kg/day) or losartan (34mg/kg/two times/day) for 60days. Testicular function parameters were evaluated from spermatozoa of the vas deferens. Testes were processed for histopathological and morphometric-stereological analysis. Proliferating cell nuclear antigen (PCNA) immunohistochemistry was evaluated. KEY FINDINGS: Radiation significantly reduced sperm motility, concentration, vitality, and increased the number of abnormal spermatozoa. Telmisartan and losartan did not significantly prevent these radiation-induced disorders. Seminiferous tubules were atrophied in both untreated and treated irradiated testes, and exhibited vacuoles, increased interstitial tissue and high number of blood vessels. However, several seminiferous tubules in recuperation were founded among damaged tubules in the testes of treated animals. The PCNA immunohistochemistry confirmed these outcomes. PCNA-positive cells were detected in dividing spermatogonia and spermatocytes from irradiated telmisartan and losartan treated rats whereas in the only-irradiated group, PCNA staining was observed in the nuclei of only the surviving spermatogonia. SIGNIFICANCE: Under these experimental conditions, the testicular function parameters showed that radiation produced marked damage that was not reversed by treatments. However, gonadal restructuring and recovery of spermatogenesis in treated animals may to reflect attenuation of radiation-induced damages and potential start of recovery.
[Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Benzimidazóis/farmacologia
Benzoatos/farmacologia
Losartan/farmacologia
Protetores contra Radiação/farmacologia
Testículo/efeitos dos fármacos
Testículo/efeitos da radiação
[Mh] Termos MeSH secundário: Animais
Masculino
Ratos Wistar
Espermatogênese/efeitos dos fármacos
Espermatogênese/efeitos da radiação
Espermatozoides/efeitos dos fármacos
Espermatozoides/patologia
Espermatozoides/efeitos da radiação
Testículo/patologia
Testículo/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Benzimidazoles); 0 (Benzoates); 0 (Radiation-Protective Agents); JMS50MPO89 (Losartan); U5SYW473RQ (telmisartan)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171231
[St] Status:MEDLINE


  4 / 8012 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29223539
[Au] Autor:Atanasova D; Tchekalarova J; Ivanova N; Nenchovska Z; Pavlova E; Atanassova N; Lazarov N
[Ad] Endereço:Institute of Neurobiology, Bulgarian Academy of Sciences, Sofia 1113, Bulgaria; Department of Anatomy, Faculty of Medicine, Trakia University, Stara Zagora 6003, Bulgaria; Department of Genes and Behavior, Max Planck Institute of Biophysical Chemistry, Göttingen 37077, Germany. Electronic address: d
[Ti] Título:Losartan suppresses the kainate-induced changes of angiotensin AT receptor expression in a model of comorbid hypertension and epilepsy.
[So] Source:Life Sci;193:40-46, 2018 Jan 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Experimental and clinical studies have demonstrated that components of renin-angiotensin system are elevated in the hippocampus in epileptogenic conditions. In the present work, we explored the changes in the expression of angiotensin II receptor, type 1 (AT receptor) in limbic structures, as well as the effect of the AT1 receptor antagonist losartan in a model of comorbid hypertension and epilepsy. MAIN METHODS: The expression of AT receptors was compared between spontaneously hypertensive rats (SHRs) and Wistar rats by using immunohistochemistry in the kainate (KA) model of temporal lobe epilepsy (TLE). The effect of losartan was studied on AT receptor expression in epileptic rats that were treated for a period of 4weeks after status epilepticus. KEY FINDINGS: The naive and epileptic SHRs were characterized by stronger protein expression of AT receptor than normotensive Wistar rats in the CA1, CA3a, CA3b, CA3c field and the hilus of the dentate gyrus of the dorsal hippocampus but fewer cells were immunostained in the piriform cortex. Increased AT immunostaining was observed in the basolateral amygdala of epileptic SHRs but not of epileptic Wistar rats. Losartan exerted stronger and structure-dependent suppression of AT receptor expression in SHRs compared to Wistar rats. SIGNIFICANCE: Our results confirm the important role of AT receptor in epilepsy and suggest that the AT receptor antagonists could be used as a therapeutic strategy for treatment of comorbid hypertension and epilepsy.
[Mh] Termos MeSH primário: Losartan/farmacologia
Receptor Tipo 1 de Angiotensina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Angiotensina II/farmacologia
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Angiotensinas
Animais
Pressão Sanguínea/efeitos dos fármacos
Comorbidade
Modelos Animais de Doenças
Epilepsia/tratamento farmacológico
Expressão Gênica/efeitos dos fármacos
Hipocampo/metabolismo
Hipertensão/tratamento farmacológico
Ácido Caínico/efeitos adversos
Ácido Caínico/metabolismo
Sistema Límbico/patologia
Losartan/metabolismo
Losartan/uso terapêutico
Masculino
Ratos
Ratos Endogâmicos SHR
Ratos Wistar
Sistema Renina-Angiotensina/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Angiotensins); 0 (Receptor, Angiotensin, Type 1); 11128-99-7 (Angiotensin II); JMS50MPO89 (Losartan); SIV03811UC (Kainic Acid)
[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:171211
[St] Status:MEDLINE


  5 / 8012 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28745698
[Au] Autor:Podzolkov VI; Tarzimanova AI
[Ad] Endereço:I.M. Sechenov First Moscow State Medical University, Moscow, Russia.
[Ti] Título:[Telmisartan in the treatment of hypertensive patients].
[Ti] Título:Telmisartan v lechenii bol'nykh arterial'noi gipertoniei..
[So] Source:Ter Arkh;89(6):110-113, 2017.
[Is] ISSN:0040-3660
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The paper highlights the use of telmisartan, one of the currently available angiotensin receptor blockers, for the treatment of patients with hypertension, metabolic syndrome, and those at high cardiovascular risk. Telmisartan treatment allows blood pressure control, provides organ protection at different stages of the cardiovascular continuum, and reduces the risk of cardiovascular diseases and death. The additional properties and pleiotropic activity of the drug determines its wide range of applications in cardiology.
[Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Benzimidazóis/farmacologia
Benzoatos/farmacologia
Doenças Cardiovasculares/tratamento farmacológico
Hipertensão/tratamento farmacológico
Síndrome Metabólica/tratamento farmacológico
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Benzimidazoles); 0 (Benzoates); U5SYW473RQ (telmisartan)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171129
[Lr] Data última revisão:
171129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.17116/terarkh2017896110-113


  6 / 8012 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28383811
[Au] Autor:Huang CY; Lee FL; Peng SF; Lin KH; Chen RJ; Ho TJ; Tsai FJ; Padma VV; Kuo WW; Huang CY
[Ad] Endereço:Translation Research Core, China Medical University Hospital, China Medical University, Taichung, Taiwan.
[Ti] Título:HSF1 phosphorylation by ERK/GSK3 suppresses RNF126 to sustain IGF-IIR expression for hypertension-induced cardiomyocyte hypertrophy.
[So] Source:J Cell Physiol;233(2):979-989, 2018 Feb.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hypertension-induced cardiac hypertrophy and apoptosis are major characteristics of early-stage heart failure (HF). Inhibition of extracellular signal-regulated kinases (ERK) efficaciously suppressed angiotensin II (ANG II)-induced cardiomyocyte hypertrophy and apoptosis by blocking insulin-like growth factor II receptor (IGF-IIR) signaling. However, the detailed mechanism by which ANG II induces ERK-mediated IGF-IIR signaling remains elusive. Here, we found that ANG II activated ERK to upregulate IGF-IIR expression via the angiotensin II type I receptor (AT R). ERK activation subsequently phosphorylates HSF1 at serine 307, leading to a secondary phosphorylation by glycogen synthase kinase III (GSK3) at serine 303. Moreover, we found that ANG II mediated ERK/GSK3-induced IGF-IIR protein stability by downregulating the E3 ubiquitin ligase of IGF-IIR RING finger protein CXXVI (RNF126). The expression of RNF126 decreased following ANG II-induced HSF1 phosphorylation, resulting in IGF-IIR protein stability and increased cardiomyocyte injury. Inhibition of GSK3 significantly alleviated ANG II-induced cardiac hypertrophy in vivo and in vitro. Taken together, these results suggest that HSF1 phosphorylation stabilizes IGF-IIR protein stability by downregulating RNF126 during cardiac hypertrophy. ANG II activates ERK/GSK3 to phosphorylate HSF1, resulting in RNF126 degradation, which stabilizes IGF-IIR protein expression and eventually results in cardiac hypertrophy. HSF1 could be a valuable therapeutic target for cardiac diseases among hypertensive patients.
[Mh] Termos MeSH primário: Cardiomegalia/etiologia
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Glicogênio Sintase Quinase 3 beta/metabolismo
Fatores de Transcrição de Choque Térmico/metabolismo
Proteínas de Choque Térmico/metabolismo
Hipertensão/complicações
Miócitos Cardíacos/enzimologia
Receptor IGF Tipo 2/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Angiotensina II/farmacologia
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Animais
Anti-Hipertensivos/farmacologia
Apoptose
Compostos de Bifenilo/farmacologia
Cardiomegalia/enzimologia
Cardiomegalia/patologia
Cardiomegalia/prevenção & controle
Linhagem Celular
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Feminino
Hipertensão/tratamento farmacológico
Hipertensão/enzimologia
Hipertensão/patologia
Cloreto de Lítio/farmacologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/patologia
Fosforilação
Estabilidade Proteica
Transporte Proteico
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Receptor Tipo 1 de Angiotensina/metabolismo
Transdução de Sinais
Tetrazóis/farmacologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Antihypertensive Agents); 0 (Biphenyl Compounds); 0 (Heat Shock Transcription Factors); 0 (Heat-Shock Proteins); 0 (Hsf1 protein, rat); 0 (Receptor, Angiotensin, Type 1); 0 (Receptor, IGF Type 2); 0 (Tetrazoles); 11128-99-7 (Angiotensin II); EC 2.3.2.27 (Rnf126 protein, rat); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Gsk3b protein, rat); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); G4962QA067 (Lithium Chloride); J0E2756Z7N (irbesartan)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25945


  7 / 8012 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28972767
[Au] Autor:Maekawa K; Adachi M; Matsuzawa Y; Zhang Q; Kuroki R; Saito Y; Shah MB
[Ad] Endereço:Department of Analytical Chemistry, Faculty of Pharmaceutical Sciences, Doshisha Women's College of Liberal Arts , Kodo, Kyotanabe, Kyoto 610-0395, Japan.
[Ti] Título:Structural Basis of Single-Nucleotide Polymorphisms in Cytochrome P450 2C9.
[So] Source:Biochemistry;56(41):5476-5480, 2017 Oct 17.
[Is] ISSN:1520-4995
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Single-nucleotide polymorphisms in drug-metabolizing cytochrome P450 (CYP) enzymes are important contributors to interindividual differences in drug metabolism leading to adverse drug reactions. Despite their extensive characterization and importance in pharmacogenetics of clinical drugs, the structural basis of CYP polymorphisms has remained scant. Here we report the crystal structures of human CYP2C9 and its polymorphic variants, *3 (I359L) and *30 (A477T), with an antihypertensive drug losartan. The structures show distinct interaction and occupation of losartan in the active site, the access channel, and the peripheral binding site. The I359L substitution located far from the active site remarkably altered the residue side chains near the active site and the access channel, whereas the T477 substitution illustrated hydrogen-bonding interaction with the reoriented side chain of Q214. The results yield structural insights into the reduced catalytic activity of the CYP2C9 variants and have important implications for understanding genetic polymorphisms in CYP-mediated drug metabolism.
[Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/metabolismo
Anti-Hipertensivos/metabolismo
Citocromo P-450 CYP2C9/genética
Losartan/metabolismo
Modelos Moleculares
Polimorfismo de Nucleotídeo Único
[Mh] Termos MeSH secundário: Alelos
Sítio Alostérico
Substituição de Aminoácidos
Bloqueadores do Receptor Tipo 1 de Angiotensina II/química
Anti-Hipertensivos/química
Sítios de Ligação
Domínio Catalítico
Cristalografia por Raios X
Citocromo P-450 CYP2C9/química
Citocromo P-450 CYP2C9/metabolismo
Seres Humanos
Ligações de Hidrogênio
Ligantes
Losartan/química
Conformação Molecular
Conformação Proteica
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Antihypertensive Agents); 0 (Ligands); EC 1.14.13.- (CYP2C9 protein, human); EC 1.14.13.- (Cytochrome P-450 CYP2C9); JMS50MPO89 (Losartan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1021/acs.biochem.7b00795


  8 / 8012 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo SciELO Brasil
[PMID]:28953991
[Au] Autor:Murad HA; Gazzaz ZJ; Ali SS; Ibraheem MS
[Ad] Endereço:Department of Pharmacology, Faculty of Medicine, Rabigh, King Abdulaziz University, Jeddah, Saudi Arabia.
[Ti] Título:Candesartan, rather than losartan, improves motor dysfunction in thioacetamide-induced chronic liver failure in rats.
[So] Source:Braz J Med Biol Res;50(11):e6665, 2017 Sep 21.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:Minimal hepatic encephalopathy is more common than the acute syndrome. Losartan, the first angiotensin-II receptor blocker (ARB), and candesartan, another widely-used ARB, have protected against developing fibrogenesis, but there is no clear data about their curative antifibrotic effects. The current study was designed to examine their effects in an already-established model of hepatic fibrosis and also their effects on the associated motor dysfunction. Low-grade chronic liver failure (CLF) was induced in 3-month old Sprague-Dawley male rats using thioacetamide (TAA, 50 mg·kg-1·day-1) intraperitoneally for 2 weeks. The TAA-CLF rats were randomly divided into five groups (n=8) treated orally for 14 days (mg·kg-1·day-1) as follows: TAA (distilled water), losartan (5 and 10 mg/kg), and candesartan (0.1 and 0.3 mg/kg). Rats were tested for rotarod and open-field tests. Serum and hepatic biochemical markers, and hepatic histopathological changes were evaluated by H&E and Masson's staining. The TAA-CLF rats showed significant increases of hepatic malondialdehyde, hepatic expression of tumor necrosis factor-α (TNF-α), and serum ammonia, alanine aminotransferase, γ-glutamyl transferase, TNF-α, and malondialdehyde levels as well as significant decreases of hepatic and serum glutathione levels. All treatments significantly reversed these changes. The histopathological changes were moderate in losartan-5 and candesartan-0.1 groups and mild in losartan-10 and candesartan-0.3 groups. Only candesartan significantly improved TAA-induced motor dysfunction. In conclusion, therapeutic antifibrotic effects of losartan and candesartan in thioacetamide-induced hepatic fibrosis in rats are possibly through angiotensin-II receptor blocking, antioxidant, and anti-inflammatory activities. Improved motor dysfunction by candesartan could be attributed to better brain penetration and slower "off-rate" from angiotensin-II receptors. Clinical trials are recommended.
[Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/uso terapêutico
Benzimidazóis/uso terapêutico
Doença Hepática Terminal/complicações
Losartan/uso terapêutico
Transtornos Motores/tratamento farmacológico
Tetrazóis/uso terapêutico
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Amônia/sangue
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Animais
Benzimidazóis/farmacologia
Modelos Animais de Doenças
Doença Hepática Terminal/patologia
Doença Hepática Terminal/fisiopatologia
Ensaio de Imunoadsorção Enzimática
Glutationa/análise
Fígado/efeitos dos fármacos
Fígado/patologia
Cirrose Hepática/complicações
Cirrose Hepática/patologia
Cirrose Hepática/fisiopatologia
Locomoção/fisiologia
Losartan/farmacologia
Masculino
Malondialdeído/análise
Transtornos Motores/etiologia
Transtornos Motores/fisiopatologia
Distribuição Aleatória
Ratos Sprague-Dawley
Reprodutibilidade dos Testes
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Tetrazóis/farmacologia
Tioacetamida
Resultado do Tratamento
Fator de Necrose Tumoral alfa/sangue
gama-Glutamiltransferase/sangue
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Benzimidazoles); 0 (Tetrazoles); 0 (Tumor Necrosis Factor-alpha); 075T165X8M (Thioacetamide); 4Y8F71G49Q (Malondialdehyde); 7664-41-7 (Ammonia); EC 2.3.2.2 (gamma-Glutamyltransferase); EC 2.6.1.2 (Alanine Transaminase); GAN16C9B8O (Glutathione); JMS50MPO89 (Losartan); S8Q36MD2XX (candesartan)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170928
[St] Status:MEDLINE


  9 / 8012 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28935030
[Au] Autor:Korhonen MJ; Robinson JG; Annis IE; Hickson RP; Bell JS; Hartikainen J; Fang G
[Ad] Endereço:Division of Pharmaceutical Outcomes and Policy, UNC Eshelman School of Pharmacy, University of North Carolina, Chapel Hill, North Carolina; National Health and Medical Research Council Centre for Research Excellence in Frailty and Healthy Ageing, Adelaide, South Australia, Australia; Centre for Medi
[Ti] Título:Adherence Tradeoff to Multiple Preventive Therapies and All-Cause Mortality After Acute Myocardial Infarction.
[So] Source:J Am Coll Cardiol;70(13):1543-1554, 2017 Sep 26.
[Is] ISSN:1558-3597
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARB), beta-blockers and statins are recommended after acute myocardial infarction (AMI). Patients may adhere to some, but not all, therapies. OBJECTIVES: The authors investigated the effect of tradeoffs in adherence to ACE inhibitors/ARBs, beta-blockers, and statins on survival among older people after AMI. METHODS: The authors identified 90,869 Medicare beneficiaries ≥65 years of age who had prescriptions for ACE inhibitors/ARBs, beta-blockers, and statins, and survived ≥180 days after AMI hospitalization in 2008 to 2010. Adherence was measured by proportion of days covered (PDC) during 180 days following hospital discharge. Mortality follow-up extended up to 18 months after this period. The authors used Cox proportional hazards models to estimate hazard ratios of mortality for groups adherent to 2, 1, or none of the therapies versus group adherent to all 3 therapies. RESULTS: Only 49% of the patients adhered (PDC ≥80%) to all 3 therapies. Compared with being adherent to all 3 therapies, multivariable-adjusted hazard ratios (95% confidence intervals [CIs]) for mortality were 1.12 (95% CI: 1.04 to 1.21) for being adherent to ACE inhibitors/ARBs and beta-blockers only, 0.98 (95% CI: 0.91 to 1.07) for ACEI/ARBs and statins only, 1.17 (95% CI: 1.10 to 1.25) beta-blockers and statins only, 1.19 (95% CI: 1.07 to 1.32) for ACE inhibitors/ARBs only, 1.32 (95% CI: 1.21 to 1.44) for beta-blockers only, 1.26 (95% CI: 1.15 to 1.38) statins only, and 1.65 (95% CI: 1.54 to 1.76) for being nonadherent (PDC <80%) to all 3 therapies. CONCLUSIONS: Patients adherent to ACE inhibitors/ARBs and statins only had similar mortality rates as those adherent to all 3 therapies, suggesting limited additional benefit for beta-blockers in patients who were adherent to statins and ACE inhibitors/ARBs. Nonadherence to ACE inhibitors/ARBs and/or statins was associated with higher mortality.
[Mh] Termos MeSH primário: Antagonistas Adrenérgicos beta/uso terapêutico
Bloqueadores do Receptor Tipo 1 de Angiotensina II/uso terapêutico
Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico
Adesão à Medicação
Infarto do Miocárdio/mortalidade
[Mh] Termos MeSH secundário: Fatores Etários
Idoso
Idoso de 80 Anos ou mais
Quimioterapia Combinada
Feminino
Hospitalização
Seres Humanos
Masculino
Medicare
Infarto do Miocárdio/tratamento farmacológico
Infarto do Miocárdio/prevenção & controle
Modelos de Riscos Proporcionais
Estados Unidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Antagonists); 0 (Angiotensin II Type 1 Receptor Blockers); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170923
[St] Status:MEDLINE


  10 / 8012 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28864378
[Au] Autor:Shamardl HA; El-Ashmony SM; Kamel HF; Fatani SH
[Ad] Endereço:Department of Pharmacology (HAS), Faculty of Medicine, Fayoum University, Fayoum, Egypt; Department of Pharmacology & Clinical Pharmacy (SME), Faculty of Pharmacy, Umm Al-Qura University, Makkah, Saudi Arabia. Electronic address: hanan2remember@yahoo.com.
[Ti] Título:Potential Cardiovascular and Renal Protective Effects of Vitamin D and Coenzyme Q in l-NAME-Induced Hypertensive Rats.
[So] Source:Am J Med Sci;354(2):190-198, 2017 Aug.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hypertension is one of the primary modifiable risk factors for cardiovascular disease. Adequate vitamin D (vit D) levels have been shown to reduce vascular smooth muscle contraction and to increase arterial compliance, which may be beneficial in hypertension. Further, coenzyme Q10 (COQ10) through its action to lower oxidative stress has been reported to have beneficial effects on hypertension and heart failure. This study examined the possible cardiac and renal protective effects of vit D and COQ10 both separately and in combination with an angiotensin II receptor blocker, valsartan (vals) in l-NAME hypertensive rats. MATERIALS AND METHODS: Hypertension was induced in rats by l-NAME administration. Following induction of hypertension, the rats were assigned into the following 6 subgroups: an l-NAME alone group and treated groups receiving the following drugs intraperitoneally for 6 weeks; vals, vit D, COQ10 and combination of vals with either vit D or COQ10. A group of normotensive rats were used as negative controls. At the end of the treatment period, blood pressure, serum creatinine, blood urea nitrogen, lipids and serum, cardiac and renal parameters of oxidative stress were measured. RESULTS: Compared to the l-NAME only group, all treatments lowered systolic, diastolic, mean arterial pressure, total cholesterol, low-density lipoprotein cholesterol, and creatinine levels as well as TNF-α and malondialdehyde. Further, the agents increased serum, cardiac and renal total antioxidant capacity. Interestingly, the combination of agents had further effects on all the parameters compared to treatment with each single agent. CONCLUSIONS: The study suggests that the additive protective effects of vit D and COQ10 when used alone or concurrent with vals treatment in hypertensive rats may be due to their effects as antioxidants, anticytokines and blood pressure conservers.
[Mh] Termos MeSH primário: Hipertensão/tratamento farmacológico
Ubiquinona/análogos & derivados
Valsartana/farmacologia
Vitamina D/farmacologia
[Mh] Termos MeSH secundário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Animais
Doenças Cardiovasculares/tratamento farmacológico
Hipertensão/induzido quimicamente
Nefropatias/tratamento farmacológico
NG-Nitroarginina Metil Éster/toxicidade
Ratos
Ratos Wistar
Ubiquinona/farmacologia
Ubiquinona/uso terapêutico
Vitamina D/uso terapêutico
Vitaminas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Vitamins); 1339-63-5 (Ubiquinone); 1406-16-2 (Vitamin D); 80M03YXJ7I (Valsartan); EJ27X76M46 (coenzyme Q10); V55S2QJN2X (NG-Nitroarginine Methyl Ester)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170908
[Lr] Data última revisão:
170908
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE



página 1 de 802 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde