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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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[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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