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[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

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[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

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[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

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[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

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[PMID]: 28859786 [Au] Autor: Bartko PE; Dal-Bianco JP; Guerrero JL; Beaudoin J; Szymanski C; Kim DH; Seybolt MM; Handschumacher MD; Sullivan S; Garcia ML; Titus JS; Wylie-Sears J; Irvin WS; Messas E; Hagège AA; Carpentier A; Aikawa E; Bischoff J; Levine RA; Leducq Transatlantic Mitral Network [Ad] Endereço: Cardiac Ultrasound Laboratory, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. [Ti] Título: Effect of Losartan on Mitral Valve Changes After Myocardial Infarction. [So] Source: J Am Coll Cardiol;70(10):1232-1244, 2017 Sep 05. [Is] ISSN: 1558-3597 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: BACKGROUND: After myocardial infarction (MI), mitral valve (MV) tethering stimulates adaptive leaflet growth, but counterproductive leaflet thickening and fibrosis augment mitral regurgitation (MR), doubling heart failure and mortality. MV fibrosis post-MI is associated with excessive endothelial-to-mesenchymal transition (EMT), driven by transforming growth factor (TGF)-ß overexpression. In vitro, losartan-mediated TGF-ß inhibition reduces EMT of MV endothelial cells. OBJECTIVES: This study tested the hypothesis that profibrotic MV changes post-MI are therapeutically accessible, specifically by losartan-mediated TGF-ß inhibition. METHODS: The study assessed 17 sheep, including 6 sham-operated control animals and 11 with apical MI and papillary muscle retraction short of producing MR; 6 of the 11 were treated with daily losartan, and 5 were untreated, with flexible epicardial mesh comparably limiting left ventricular (LV) remodeling. LV volumes, tethering, and MV area were quantified by using three-dimensional echocardiography at baseline and at 60 ± 6 days, and excised leaflets were analyzed by histopathology and flow cytometry. RESULTS: Post-MI LV dilation and tethering were comparable in the losartan-treated and untreated LV constraint sheep. Telemetered sensors (n = 6) showed no significant losartan-induced changes in arterial pressure. Losartan strongly reduced leaflet thickness (0.9 ± 0.2 mm vs. 1.6 ± 0.2 mm; p < 0.05; 0.4 ± 0.1 mm sham animals), TGF-ß, and downstream phosphorylated extracellular-signal-regulated kinase and EMT (27.2 ± 12.0% vs. 51.6 ± 11.7% α-smooth muscle actin-positive endothelial cells, p < 0.05; 7.2 ± 3.5% sham animals), cellular proliferation, collagen deposition, endothelial cell activation (vascular cell adhesion molecule-1 expression), neovascularization, and cells positive for cluster of differentiation (CD) 45, a hematopoietic marker associated with post-MI valve fibrosis. Leaflet area increased comparably (17%) in constrained and losartan-treated sheep. CONCLUSIONS: Profibrotic changes of tethered MV leaflets post-MI can be modulated by losartan without eliminating adaptive growth. Understanding the cellular and molecular mechanisms could provide new opportunities to reduce ischemic MR. [Mh] Termos MeSH primário: Losartan/farmacologia Insuficiência da Valva Mitral/diagnóstico Valva Mitral/efeitos dos fármacos Infarto do Miocárdio/tratamento farmacológico [Mh] Termos MeSH secundário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia Animais Modelos Animais de Doenças Ecocardiografia Tridimensional Células Endoteliais/metabolismo Células Endoteliais/patologia Fibrose Seres Humanos Valva Mitral/diagnóstico por imagem Insuficiência da Valva Mitral/etiologia Insuficiência da Valva Mitral/fisiopatologia Infarto do Miocárdio/complicações Infarto do Miocárdio/fisiopatologia Músculos Papilares/diagnóstico por imagem Músculos Papilares/efeitos dos fármacos Ovinos Fator de Crescimento Transformador beta/metabolismo Remodelação Ventricular [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Angiotensin II Type 1 Receptor Blockers); 0 (Transforming Growth Factor beta); JMS50MPO89 (Losartan) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 171111 [Lr] Data última revisão: 171111 [Sb] Subgrupo de revista: AIM; IM [Da] Data de entrada para processamento: 170902 [St] Status: MEDLINE

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[PMID]: 28843962 [Au] Autor: Chao Y; Zhu L; Qu X; Zhang J; Zhang J; Kong X; Gu Y; Pu J; Wu W; Ye P; Luo J; Yang H; Chen S [Ad] Endereço: Department of Cardiology, Nanjing First Hospital, Nanjing Medical University, Nanjing, China. [Ti] Título: Inhibition of angiotension II type 1 receptor reduced human endothelial inflammation induced by low shear stress. [So] Source: Exp Cell Res;360(2):94-104, 2017 Nov 15. [Is] ISSN: 1090-2422 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Low shear stress (LSS)-induced endothelial inflammation is the basis for the development of atherosclerosis. However, the mechanism underlying LSS-induced inflammation is not well understood. The angiotensin II type 1 receptor (AT1R), a component of the renin-angiotensin system, participates in atherosclerotic plaque progression. The aim of this study was to investigate the role of AT1R in LSS-induced endothelial activation. Using immunohistochemistry, we noted significant increases in AT1R, vascular endothelial adhesion cell-1 (VCAM1), and intercellular adhesion molecule-1 (ICAM1) expression in the inner curvature of the aortic arch in C57BL/6 mice compared to the descending aorta in these mice. Moreover, western blotting revealed that these LSS-induced increases in AT1R, ICAM1 and VCAM1 expression were time dependent. However, the expression of these proteins was significantly abolished by treatment with the AT1R antagonist Losartan (1µM) or AT1R small interfering RNA (siRNA). AT1R inhibition significantly suppressed extracellular signal-regulated kinase 1/2 (ERK) upregulation, which also resulted in decreases in ICAM1 and VCAM1 protein expression. These findings demonstrate that LSS induces endothelial inflammation via AT1R/ERK signaling and that Losartan has beneficial effects on endothelial inflammation. [Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos Inflamação/etiologia Inflamação/prevenção & controle Losartan/farmacologia Estresse Mecânico [Mh] Termos MeSH secundário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/uso terapêutico Animais Células Cultivadas Endotélio Vascular/efeitos dos fármacos Endotélio Vascular/patologia Células Endoteliais da Veia Umbilical Humana/imunologia Células Endoteliais da Veia Umbilical Humana/patologia Seres Humanos Losartan/uso terapêutico Camundongos Camundongos Endogâmicos C57BL RNA Interferente Pequeno/farmacologia RNA Interferente Pequeno/uso terapêutico Receptor Tipo 1 de Angiotensina/genética Receptor Tipo 1 de Angiotensina/metabolismo Resistência ao Cisalhamento/efeitos dos fármacos Vasculite/patologia Vasculite/prevenção & controle [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Angiotensin II Type 1 Receptor Blockers); 0 (RNA, Small Interfering); 0 (Receptor, Angiotensin, Type 1); JMS50MPO89 (Losartan) [Em] Mês de entrada: 1711 [Cu] Atualização por classe: 171103 [Lr] Data última revisão: 171103 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170828 [St] Status: MEDLINE

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[PMID]: 28827087 [Au] Autor: Smeda JS; Daneshtalab N [Ad] Endereço: Division of BioMedical Sciences, Memorial University of Newfoundland, St. John's, Newfoundland, Canada. Electronic address: jsmeda@mun.ca. [Ti] Título: Cerebrovascular recovery after stroke with individual and combined losartan and captopril treatment of SHRsp. [So] Source: Vascul Pharmacol;96-98:40-52, 2017 Sep. [Is] ISSN: 1879-3649 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: We assessed whether the superior restoration of cerebrovascular function after hemorrhagic stroke by losartan versus captopril treatment was due to better BP, uremia, uricaemia, or aldosterone control in Kyoto Wistar stroke-prone-hypertensive rats and evaluated whether elevated angiotensin II (A2) levels enhanced the effectiveness of losartan treatment. Constriction was studied in the middle cerebral arteries (MCAs) using a pressure myograph. Post-stroke survival increased from 21 to 310 and 189days respectively with losartan and captopril treatment. Neither treatment reduced BP, both reversed uremia and hyperaldosteronism equally after 7days. Plasma uric acid remained low. At stroke, MCA constriction to pressure (PDC), protein kinase C (PKC) activation, depolarization, and sarcoplasmic Ca were attenuated. Endothelial-dependent-vasodilation by bradykinin and endogenous NO release were lost. Both treatments recovered these functions within 7days. These functions deteriorated after 116days of captopril but not losartan treatment. Inhibiting A2 formation during losartan treatment didn't alter BP or vascular recovery. The superior recovery of PDC by losartan over captopril was not produced by better BP, uremia or aldosterone control or elevated A2. PDC recovery was associated with improved PKC function and enhanced basal NO release. The re-establishment of PDC could reduce cerebrovascular over-perfusion and hematoma expansion after stroke. [Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia Inibidores da Enzima Conversora de Angiotensina/farmacologia Captopril/farmacologia Circulação Cerebrovascular/efeitos dos fármacos Hipertensão/complicações Infarto da Artéria Cerebral Média/tratamento farmacológico Losartan/farmacologia Artéria Cerebral Média/efeitos dos fármacos [Mh] Termos MeSH secundário: Aldosterona/sangue Animais Pressão Sanguínea/efeitos dos fármacos Modelos Animais de Doenças Combinação de Medicamentos Ativação Enzimática Hipertensão/sangue Hipertensão/metabolismo Infarto da Artéria Cerebral Média/sangue Infarto da Artéria Cerebral Média/etiologia Infarto da Artéria Cerebral Média/fisiopatologia Artéria Cerebral Média/metabolismo Artéria Cerebral Média/fisiopatologia Óxido Nítrico/metabolismo Proteína Quinase C/metabolismo Ratos Endogâmicos SHR Ratos Endogâmicos WKY Sistema Renina-Angiotensina/efeitos dos fármacos Fatores de Tempo Ureia/sangue Ácido Úrico/sangue Vasoconstrição/efeitos dos fármacos [Pt] Tipo de publicação: COMPARATIVE STUDY; JOURNAL ARTICLE [Nm] Nome de substância: 0 (Angiotensin II Type 1 Receptor Blockers); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Drug Combinations); 268B43MJ25 (Uric Acid); 31C4KY9ESH (Nitric Oxide); 4964P6T9RB (Aldosterone); 8W8T17847W (Urea); 9G64RSX1XD (Captopril); EC 2.7.11.13 (Protein Kinase C); JMS50MPO89 (Losartan) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171030 [Lr] Data última revisão: 171030 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170823 [St] Status: MEDLINE

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[PMID]: 28734043 [Au] Autor: Manini TM; Anton SD; Beavers DP; Cauley JA; Espeland MA; Fielding RA; Kritchevsky SB; Leeuwenburgh C; Lewis KH; Liu C; McDermott MM; Miller ME; Tracy RP; Walston JD; Radziszewska B; Lu J; Stowe C; Wu S; Newman AB; Ambrosius WT; Pahor M; ENRGISE Pilot study investigators [Ad] Endereço: Department of Aging and Geriatric Research, University of Florida, Gainesville, Florida. [Ti] Título: ENabling Reduction of Low-grade Inflammation in SEniors Pilot Study: Concept, Rationale, and Design. [So] Source: J Am Geriatr Soc;65(9):1961-1968, 2017 Sep. [Is] ISSN: 1532-5415 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: OBJECTIVES: To test two interventions to reduce interleukin (IL)-6 levels, an indicator of low-grade chronic inflammation and an independent risk factor for impaired mobility and slow walking speed in older adults. DESIGN: The ENabling Reduction of low-Grade Inflammation in SEniors (ENRGISE) Pilot Study was a multicenter, double-blind, placebo-controlled randomized pilot trial of two interventions to reduce IL-6 levels. SETTING: Five university-based research centers. PARTICIPANTS: Target enrollment was 300 men and women aged 70 and older with an average plasma IL-6 level between 2.5 and 30 pg/mL measured twice at least 1 week apart. Participants had low to moderate physical function, defined as self-reported difficulty walking one-quarter of a mile or climbing a flight of stairs and usual walk speed of less than 1 m/s on a 4-m usual-pace walk. INTERVENTION: Participants were randomized to losartan, omega-3 fish oil (ω-3), combined losartan and ω-3, or placebo. Randomization was stratified depending on eligibility for each group. A titration schedule was implemented to reach a dose that was safe and effective for IL-6 reduction. Maximal doses were 100 mg/d for losartan and 2.8 g/d for ω-3. MEASUREMENTS: IL-6, walking speed over 400 m, physical function (Short Physical Performance Battery), other inflammatory markers, safety, tolerability, frailty domains, and maximal leg strength were measured. RESULTS: Results from the ENRGISE Pilot Study will provide recruitment yields, feasibility, medication tolerance and adherence, and preliminary data to help justify a sample size for a more definitive randomized trial. CONCLUSION: The ENRGISE Pilot Study will inform a larger subsequent trial that is expected to have important clinical and public health implications for the growing population of older adults with low-grade chronic inflammation and mobility limitations. [Mh] Termos MeSH primário: Inflamação/prevenção & controle Interleucina-6 Limitação da Mobilidade [Mh] Termos MeSH secundário: Idoso Anti-Hipertensivos/uso terapêutico Método Duplo-Cego Ácido Eicosapentaenoico/uso terapêutico Feminino Seres Humanos Interleucina-6/sangue Losartan/uso terapêutico Masculino Projetos Piloto [Pt] Tipo de publicação: JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL [Nm] Nome de substância: 0 (Antihypertensive Agents); 0 (Interleukin-6); AAN7QOV9EA (Eicosapentaenoic Acid); JMS50MPO89 (Losartan) [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 171018 [Lr] Data última revisão: 171018 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170723 [St] Status: MEDLINE [do] DOI: 10.1111/jgs.14965

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[PMID]: 28712765 [Au] Autor: de Queiroz DB; Ramos-Alves FE; Santos-Rocha J; Duarte GP; Xavier FE [Ad] Endereço: Departamento de Fisiologia e Farmacologia, Universidade Federal de Pernambuco, Recife, Brazil. [Ti] Título: Losartan reverses COX-2-dependent vascular dysfunction in offspring of hyperglycaemic rats. [So] Source: Life Sci;184:71-80, 2017 Sep 01. [Is] ISSN: 1879-0631 [Cp] País de publicação: Netherlands [La] Idioma: eng [Ab] Resumo: AIMS: This study examined whether chronic treatment with losartan, an angiotensin II type 1 receptor (AT R) antagonist, might reverse COX-2-mediated vascular dysfunction in mesenteric resistance arteries (MRA) from offspring of hyperglycaemic rats. MATERIALS AND METHODS: Male 12-month-old offspring of hyperglycaemic (O-DR) and normoglycaemic (O-CR) rats were treated with losartan (15mg·kg·day ) during 2months. Third order MRA of untreated and losartan-treated O-DR and O-CR were mounted in wire myograph for isometric tension measurements. COX-2 expression was analyzed by Western blot; TxA , PGE and PGF release was measured using commercial kits. KEY FINDINGS: O-DR showed increased blood pressure, impaired acetylcholine-induced vasodilation and increased noradrenaline-induced vasoconstriction than O-CR. All these parameters were normalized by losartan in O-DR. Pre-incubation of MRA with indomethacin (COX-1/2 inhibitor), NS-398 (COX-2 inhibitor) or tempol (superoxide dismutase mimetic) increased relaxation to acetylcholine and reduced contraction to noradrenaline only in O-DR. COX-2 expression, TxA , PGE and PGF release were increased in O-DR. In losartan-treated O-DR, NS-398, indomethacin or tempol failed to produce any effect on acetylcholine or noradrenaline responses. Losartan treatment reduced COX-2 expression, TxA , PGE and PGF release in O-DR. SIGNIFICANCE: The present results reveal that chronic losartan administration in O-DR normalizes endothelial function in MRA by correcting the existing COX-2 overexpression and the imbalance between endothelium-derived relaxing and contracting factors. These findings not only support the beneficial effects of AT receptor antagonist in O-DR, but also suggest the implication of angiotensin II as a putative mediator of hyperglycemia-programmed vascular dysfunction in rats. [Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia Ciclo-Oxigenase 2/metabolismo Hiperglicemia/complicações Losartan/farmacologia Artérias Mesentéricas/efeitos dos fármacos [Mh] Termos MeSH secundário: Angiotensina II/metabolismo Bloqueadores do Receptor Tipo 1 de Angiotensina II/administração & dosagem Animais Endotélio Vascular/efeitos dos fármacos Endotélio Vascular/patologia Feminino Losartan/administração & dosagem Masculino Artérias Mesentéricas/patologia Gravidez Ratos Ratos Wistar Vasoconstrição/efeitos dos fármacos Vasodilatação/efeitos dos fármacos [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Angiotensin II Type 1 Receptor Blockers); 11128-99-7 (Angiotensin II); EC 1.14.99.1 (Cyclooxygenase 2); JMS50MPO89 (Losartan) [Em] Mês de entrada: 1708 [Cu] Atualização por classe: 170815 [Lr] Data última revisão: 170815 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170718 [St] Status: MEDLINE

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MEDLINE

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[PMID]: 28679681 [Au] Autor: Azevedo ER; Mak S; Floras JS; Parker JD [Ad] Endereço: Division of Cardiology, Department of Medicine, Mount Sinai Hospital, Toronto, Ontario, Canada; Lunenfeld-Tanenbaum Research Institute, University of Toronto, Toronto, Ontario, Canada; and Department of Pharmacology and Toxicology, University of Toronto, Toronto, Ontario, Canada. [Ti] Título: Acute effects of angiotensin-converting enzyme inhibition versus angiotensin II receptor blockade on cardiac sympathetic activity in patients with heart failure. [So] Source: Am J Physiol Regul Integr Comp Physiol;313(4):R410-R417, 2017 Oct 01. [Is] ISSN: 1522-1490 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: The beneficial effects of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (ANG II) receptor antagonists in patients with heart failure secondary to reduced ejection fraction (HFrEF) are felt to result from prevention of the adverse effects of ANG II on systemic afterload and renal homeostasis. However, ANG II can activate the sympathetic nervous system, and part of the beneficial effects of ACE inhibitors and ANG II antagonists may result from their ability to inhibit such activation. We examined the acute effects of the ACE inhibitor captopril (25 mg, = 9) and the ANG II receptor antagonist losartan (50 mg, = 10) on hemodynamics as well as total body and cardiac norepinephrine spillover in patients with chronic HFrEF. Hemodynamic and neurochemical measurements were made at baseline and at 1, 2, and 4 h after oral dosing. Administration of both drugs caused significant reductions in systemic arterial, cardiac filling, and pulmonary artery pressures ( < 0.05 vs. baseline). There was no significant difference in the magnitude of those hemodynamic effects. Plasma concentrations of ANG II were significantly decreased by captopril and increased by losartan ( < 0.05 vs. baseline for both). Total body sympathetic activity increased in response to both captopril and losartan ( < 0.05 vs. baseline for both); however, there was no change in cardiac sympathetic activity in response to either drug. The results of the present study do not support the hypothesis that the acute inhibition of the renin-angiotensin system has sympathoinhibitory effects in patients with chronic HFrEF. [Mh] Termos MeSH primário: Antagonistas de Receptores de Angiotensina/farmacologia Inibidores da Enzima Conversora de Angiotensina/farmacologia Captopril/farmacologia Insuficiência Cardíaca/tratamento farmacológico Coração/efeitos dos fármacos Losartan/farmacologia Sistema Nervoso Simpático/efeitos dos fármacos [Mh] Termos MeSH secundário: Idoso Antagonistas de Receptores de Angiotensina/uso terapêutico Inibidores da Enzima Conversora de Angiotensina/uso terapêutico Captopril/uso terapêutico Feminino Coração/fisiopatologia Insuficiência Cardíaca/fisiopatologia Hemodinâmica/efeitos dos fármacos Hemodinâmica/fisiologia Seres Humanos Losartan/uso terapêutico Masculino Meia-Idade Sistema Renina-Angiotensina/efeitos dos fármacos Sistema Renina-Angiotensina/fisiologia Sistema Nervoso Simpático/fisiopatologia Resultado do Tratamento [Pt] Tipo de publicação: COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL [Nm] Nome de substância: 0 (Angiotensin Receptor Antagonists); 0 (Angiotensin-Converting Enzyme Inhibitors); 9G64RSX1XD (Captopril); JMS50MPO89 (Losartan) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171019 [Lr] Data última revisão: 171019 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 170707 [St] Status: MEDLINE [do] DOI: 10.1152/ajpregu.00095.2017

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