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Pesquisa : D12.644.456.073.041.815 [Categoria DeCS]
Referências encontradas : 285 [refinar]
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[PMID]:25108041
[Au] Autor:Speth RC; Vento PJ; Carrera EJ; Gonzalez-Reily L; Linares A; Santos K; Swindle JD; Daniels D
[Ad] Endereço:Department of Pharmaceutical Sciences, College of Pharmacy, Nova Southeastern University, Fort Lauderdale, FL 33328, USA; Department of Pharmacology and Physiology, College of Medicine, Georgetown University, Washington, DC 20057, USA. Electronic address: rs1251@nova.edu.
[Ti] Título:Acute repeated intracerebroventricular injections of angiotensin II reduce agonist and antagonist radioligand binding in the paraventricular nucleus of the hypothalamus and median preoptic nucleus in the rat brain.
[So] Source:Brain Res;1583:132-40, 2014 Oct 02.
[Is] ISSN:1872-6240
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Angiotensin II (Ang II) stimulates water and saline intakes when injected into the brain of rats. This arises from activation of the AT1 Ang II receptor subtype. Acute repeated injections, however, decrease the water intake response to Ang II without affecting saline intake. Previous studies provide evidence that Ang II-induced water intake is mediated via the classical G protein coupling pathway, whereas the saline intake caused by Ang II is mediated by an ERK 1/2 MAP kinase signaling pathway. Accordingly, the different behavioral response to repeated injections of Ang II may reflect a selective effect on G protein coupling. To test this hypothesis, we examined the binding of a radiolabeled agonist ((125)I-sarcosine(1) Ang II) and a radiolabeled antagonist ((125)I-sarcosine(1), isoleucine(8) Ang II) in brain homogenates and tissue sections prepared from rats given repeated injections of Ang II or vehicle. Although no treatment-related differences were found in hypothalamic homogenates, a focus on specific brain structures using receptor autoradiography, found that the desensitization treatment reduced binding of both radioligands in the paraventricular nucleus of the hypothalamus (PVN) and median preoptic nucleus (MnPO), but not in the subfornical organ (SFO). Because G protein coupling is reported to have a selective effect on agonist binding without affecting antagonist binding, these findings do not support a G protein uncoupling treatment effect. This suggests that receptor number is more critical to the water intake response than the saline intake response, or that pathways downstream from the G protein mediate desensitization of the water intake response.
[Mh] Termos MeSH primário: Angiotensina II/farmacologia
Fármacos do Sistema Nervoso Central/farmacologia
Núcleo Hipotalâmico Paraventricular/efeitos dos fármacos
Área Pré-Óptica/efeitos dos fármacos
[Mh] Termos MeSH secundário: 1-Sarcosina-8-Isoleucina Angiotensina II/metabolismo
Angiotensina II/administração & dosagem
Angiotensina II/análogos & derivados
Angiotensina II/metabolismo
Bloqueadores do Receptor Tipo 1 de Angiotensina II/metabolismo
Bloqueadores do Receptor Tipo 2 de Angiotensina II/metabolismo
Animais
Ingestão de Líquidos/efeitos dos fármacos
Ingestão de Líquidos/fisiologia
Água Potável/administração & dosagem
Radioisótopos do Iodo
Masculino
Núcleo Hipotalâmico Paraventricular/metabolismo
Área Pré-Óptica/fisiopatologia
Ensaio Radioligante
Compostos Radiofarmacêuticos
Ratos Sprague-Dawley
Receptor Tipo 2 de Angiotensina/agonistas
Receptor Tipo 2 de Angiotensina/metabolismo
Cloreto de Sódio na Dieta/administração & dosagem
Órgão Subfornical/efeitos dos fármacos
Órgão Subfornical/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Angiotensin II Type 2 Receptor Blockers); 0 (Central Nervous System Agents); 0 (Drinking Water); 0 (Iodine Radioisotopes); 0 (Radiopharmaceuticals); 0 (Receptor, Angiotensin, Type 2); 0 (Sodium Chloride, Dietary); 11128-99-7 (Angiotensin II); 59680-38-5 (angiotensin II, Sar(1)-); 9088-01-1 (1-Sarcosine-8-Isoleucine Angiotensin II)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140810
[St] Status:MEDLINE


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[PMID]:25036239
[Au] Autor:Thatcher S
[Ad] Endereço:University of Kentucky, Lexington, KY, USA. Electronic address: SeanThatcher@uky.edu.
[Ti] Título:Commentary for Clancy, P et al., ARBs and ERK activation: new insights on human atherosclerosis.
[So] Source:Atherosclerosis;236(1):131-2, 2014 Sep.
[Is] ISSN:1879-1484
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Mh] Termos MeSH primário: 1-Sarcosina-8-Isoleucina Angiotensina II/farmacologia
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Compostos de Bifenilo/farmacologia
Citocinas/secreção
Endotélio Vascular/efeitos dos fármacos
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Peptídeos/farmacologia
Sistema Renina-Angiotensina/efeitos dos fármacos
Tetrazóis/farmacologia
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Biphenyl Compounds); 0 (Cytokines); 0 (DX600 peptide); 0 (Peptides); 0 (Tetrazoles); 9088-01-1 (1-Sarcosine-8-Isoleucine Angiotensin II); EC 2.7.11.24 (MAPK1 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); J0E2756Z7N (irbesartan)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140719
[St] Status:MEDLINE


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[PMID]:25016365
[Au] Autor:Clancy P; Koblar SA; Golledge J
[Ad] Endereço:Health Practitioners And Researchers Together-Blood, Endothelium And Tissue (HART-BEAT), Australian Institute for Tropical Health and Medicine (AITHM), School of Veterinary and Biomedical Sciences, James Cook University, Townsville, Queensland 4811, Australia. Electronic address: paula.clancy@jcu.edu.au.
[Ti] Título:Angiotensin receptor 1 blockade reduces secretion of inflammation associated cytokines from cultured human carotid atheroma and vascular cells in association with reduced extracellular signal regulated kinase expression and activation.
[So] Source:Atherosclerosis;236(1):108-15, 2014 Sep.
[Is] ISSN:1879-1484
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: A number of studies have suggested that angiotensin II (AII) receptor type 1 (ATR1) blocking drugs (ARBs) have anti-inflammatory effects however the mechanisms responsible are poorly investigated. OBJECTIVE: To determine the role of extracellular signal regulated kinase (ERK)1/2 in ARB induced anti-inflammatory effects within human carotid atherosclerosis. METHODS: Atheroma samples obtained from patients undergoing carotid endarterectomy were cultured with and without ATR1 (irbesartan), ERK1/2 (PD98059), AII ([Sar(1), Ile(8)]-AII) and angiotensin converting enzyme (ACE)2 (DX600) blockade. The in vitro effects of ATR1 and ERK1/2 blockade and exogenous AII on serum stimulated healthy, primary vascular cells were also investigated. Outcome was assessed by measuring cytokine, (interleukin (IL)-6, IL-8, C-C motif chemokine (CCL)2, C-X-C motif chemokine (CXCL)5, osteoprotegerin (OPG), osteopontin (OPN), CXCL16), concentrations in supernatants and phosphorylated ERK1/2 in the tissue lysates using ELISA. ERK1/2 expression in the tissue was assessed using Western blotting. RESULTS: Irbesartan reduced concentrations of IL-6, IL-8, CCL2, CXCL5, OPG, OPN and CXCL16 in both atheroma and primary vascular cell culture supernatants. The reduction in cytokine levels in the atheroma supernatant was correlated to a reduction in ERK1/2 expression in the tissue. Inhibition of ERK1/2 downregulated IL-6, IL-8 and CXCL5 in both atheroma and cell culture supernatants. AII and ACE2 blockade had no impact on cytokine or active ERK1/2 levels in the atheroma culture. CONCLUSION: Our findings suggest that ATR1 blockade downregulates atheroma tissue ERK1/2 expression leading to a reduction in cytokine production and that a non-AII agonist ATR1 signalling response may induce expression of these inflammation associated cytokines in the atheroma.
[Mh] Termos MeSH primário: 1-Sarcosina-8-Isoleucina Angiotensina II/farmacologia
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Compostos de Bifenilo/farmacologia
Citocinas/secreção
Endotélio Vascular/efeitos dos fármacos
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Peptídeos/farmacologia
Sistema Renina-Angiotensina/efeitos dos fármacos
Tetrazóis/farmacologia
[Mh] Termos MeSH secundário: Idoso
Artérias Carótidas/patologia
Células Cultivadas
Quimiocinas/secreção
Endotélio Vascular/enzimologia
Endotélio Vascular/secreção
Ativação Enzimática/efeitos dos fármacos
Indução Enzimática/efeitos dos fármacos
Feminino
Seres Humanos
Inflamação
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Masculino
Meia-Idade
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/genética
Osteoprotegerina/secreção
Placa Aterosclerótica/patologia
Sistema Renina-Angiotensina/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Biphenyl Compounds); 0 (Chemokines); 0 (Cytokines); 0 (DX600 peptide); 0 (Osteoprotegerin); 0 (Peptides); 0 (TNFRSF11B protein, human); 0 (Tetrazoles); 9088-01-1 (1-Sarcosine-8-Isoleucine Angiotensin II); EC 2.7.11.24 (MAPK1 protein, human); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); J0E2756Z7N (irbesartan)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140714
[St] Status:MEDLINE


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[PMID]:22681254
[Au] Autor:Godin CM; Ferguson SS
[Ad] Endereço:J. Allyn Taylor Centre for Cell Biology, Molecular Brain Research Group, Robarts Research Institute and the Department of Physiology & Pharmacology, The University of Western Ontario 100 Perth Dr. London, Ontario, N6A 5K8, Canada.
[Ti] Título:Biased agonism of the angiotensin II type 1 receptor.
[So] Source:Mini Rev Med Chem;12(9):812-6, 2012 Aug.
[Is] ISSN:1875-5607
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:G protein-coupled receptors (GPCRs) can be activated by multiple ligands and exhibit the capacity to couple to numerous intracellular signal transduction pathways. This property allows GPCRs to be modulated by biased agonists that selectively activate specific subsets of GPCR-regulated cellular signaling proteins. The angiotensin II type 1 receptor (AT1R) is a GPCR that endogenously binds to the peptide ligand angiotensin II. More recently it has been demonstrated that a modified peptide, [Sar1I-le4-Ile8]-angiotensin II (SII) acts as a biased agonist towards the AT1R. SII binds to the AT1R without promoting heterotrimeric G protein-coupling, but serves to link the receptor to the beta-arrestin-dependent activation of the mitogen activated protein kinase pathway. The present mini-review summarizes current knowledge regarding the role of biased agonists in stimulating biased AT1R signaling.
[Mh] Termos MeSH primário: 1-Sarcosina-8-Isoleucina Angiotensina II/farmacologia
Angiotensina II/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Receptor Tipo 1 de Angiotensina/agonistas
[Mh] Termos MeSH secundário: 1-Sarcosina-8-Isoleucina Angiotensina II/metabolismo
Angiotensina II/metabolismo
Bloqueadores do Receptor Tipo 1 de Angiotensina II/metabolismo
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Arrestinas/metabolismo
Células HEK293
Seres Humanos
Ligantes
Losartan/metabolismo
Losartan/farmacologia
Conformação Proteica
Receptor Tipo 1 de Angiotensina/metabolismo
Estresse Mecânico
beta-Arrestinas
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Arrestins); 0 (Ligands); 0 (Receptor, Angiotensin, Type 1); 0 (beta-Arrestins); 11128-99-7 (Angiotensin II); 9088-01-1 (1-Sarcosine-8-Isoleucine Angiotensin II); JMS50MPO89 (Losartan)
[Em] Mês de entrada:1210
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120612
[St] Status:MEDLINE


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[PMID]:20861168
[Au] Autor:Rashid M; Arumugam TV; Karamyan VT
[Ad] Endereço:Department of Pharmaceutical Sciences and Vascular Drug Research Center, School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo, Texas 79106, USA.
[Ti] Título:Association of the novel non-AT1, non-AT2 angiotensin binding site with neuronal cell death.
[So] Source:J Pharmacol Exp Ther;335(3):754-61, 2010 Dec.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have discovered a non-AT(1), non-AT(2) angiotensin binding site in rodent and human brain membranes, which, based on its pharmacological/biochemical properties and tissue distribution, is different from angiotensin receptors and key proteases processing angiotensins. In this study, the novel angiotensin binding site was localized to a specific brain cell type by using radioligand receptor binding assays. Our results indicate that the novel binding site is expressed in mouse primary cortical neuronal membranes but not in primary cortical astroglial and bEnd.3 brain capillary endothelial cell membranes. Whole-cell binding assays in neurons showed that the binding site faces the outer side of the plasma membrane. Consistent with our previous observations, the novel binding site was unmasked by the sulfhydryl reagent p-chloromercuribenzoate. This effect had a bell-shaped curve and was reversed by reduced glutathione, indicating that the function of the binding site might be regulated by the redox state of the environment. Density of the novel binding site measured by saturation binding assays was significantly increased in neuronal membranes of cells challenged in four in vitro models of cell death (oxygen-glucose deprivation, sodium azide-induced hypoxia, N-methyl-D-aspartate neurotoxicity, and hydrogen peroxide neurotoxicity). In addition, our in vivo data from developing mouse brains showed that the density of the novel angiotensin binding site changes similarly to the pattern of neuronal death in maturating brain. This is the first time that evidence is provided on the association of the novel angiotensin binding site with neuronal death, and future studies directed toward understanding of the functions of this protein are warranted.
[Mh] Termos MeSH primário: Neurônios/citologia
Neurônios/metabolismo
Receptores de Angiotensina/metabolismo
[Mh] Termos MeSH secundário: 1-Sarcosina-8-Isoleucina Angiotensina II/metabolismo
4-Cloromercuriobenzenossulfonato/farmacologia
Angiotensina II/metabolismo
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Bloqueadores do Receptor Tipo 2 de Angiotensina II/farmacologia
Animais
Morte Celular/efeitos dos fármacos
Morte Celular/fisiologia
Membrana Celular/efeitos dos fármacos
Membrana Celular/metabolismo
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Córtex Cerebral/citologia
Córtex Cerebral/metabolismo
Feminino
Glutationa/farmacologia
Dissulfeto de Glutationa/farmacologia
Cinética
Camundongos
Camundongos Endogâmicos
Neurônios/efeitos dos fármacos
Prosencéfalo/citologia
Prosencéfalo/embriologia
Prosencéfalo/crescimento & desenvolvimento
Prosencéfalo/metabolismo
Ligação Proteica/efeitos dos fármacos
Ligação Proteica/fisiologia
Receptores de Superfície Celular/antagonistas & inibidores
Receptores de Superfície Celular/metabolismo
Frações Subcelulares/efeitos dos fármacos
Frações Subcelulares/metabolismo
Temperatura Ambiente
Ácido p-Cloromercurobenzoico/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Angiotensin II Type 2 Receptor Blockers); 0 (Receptors, Angiotensin); 0 (Receptors, Cell Surface); 11128-99-7 (Angiotensin II); 59-85-8 (p-Chloromercuribenzoic Acid); 5YIN07W42H (4-Chloromercuribenzenesulfonate); 9088-01-1 (1-Sarcosine-8-Isoleucine Angiotensin II); GAN16C9B8O (Glutathione); ULW86O013H (Glutathione Disulfide)
[Em] Mês de entrada:1102
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100924
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.110.171439


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[PMID]:20524779
[Au] Autor:Siebelmann M; Wensing J; Verspohl EJ
[Ad] Endereço:Department of Pharmacology, Institute of Medicinal Chemistry, University of Muenster, Münster, Germany.
[Ti] Título:The impact of ANG II and IV on INS-1 cells and on blood glucose and plasma insulin.
[So] Source:J Recept Signal Transduct Res;30(4):234-45, 2010 Aug.
[Is] ISSN:1532-4281
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The impact of angiotensin (ANG) for peripheral, global effects is well known. Local ANG systems including that of the insulin-releasing beta cell are not well investigated. In insulin-secreting cell line (INS-1), AT(1) and AT(4) receptors for ANG II and IV were demonstrated by Western blots. Only small amounts of ANG II-binding sites of low affinity were observed. ANG II and SARILE displaced binding of (125)I-ANG II. ANG II and IV as well as their non-degradable analogs SARILE and Nle-ANG IV increased the glucose-induced insulin release in a bell-shaped way; the maximum effect was at approximately 1 nM. The increase was antagonized by 1 microM losartan or 10 microM divalinal (AT(1) and AT(4) receptor antagonists, respectively). The insulin release was accompanied by a (45)Ca(2+) uptake in the case of ANG II and ANG IV. Divalinal abolished the effect of ANG IV and Nle-ANG IV on this parameter. ANG IV reduced the increase in blood glucose during a glucose tolerance test with corresponding, albeit smaller effects on plasma insulin. Using confocal laser scanning microscopy, transfected insulin-regulated aminopeptidase (IRAP) with AT(4) receptors was shown to be accumulated close to the nucleus and the cytosolic membrane, whereas GLUT4 was not detectable. IRAP was inhibited by ANG IV. In conclusion, AT(1) and AT(4) receptors may be involved in diabetic homeostasis. Effects are mediated by insulin release, which is accompanied by an influx of extracellular Ca(2+). The impact of ANG IV/IRAP agonists may be worth being used as antidiabetics.
[Mh] Termos MeSH primário: Angiotensina II/análogos & derivados
Glicemia/efeitos dos fármacos
Insulina/sangue
[Mh] Termos MeSH secundário: 1-Sarcosina-8-Isoleucina Angiotensina II/farmacologia
Angiotensina II/farmacologia
Animais
Western Blotting
Linhagem Celular
Cistinil Aminopeptidase/antagonistas & inibidores
Cistinil Aminopeptidase/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Glucose/farmacologia
Insulina/secreção
Losartan/farmacologia
Macrolídeos/farmacologia
Inibidor 1 de Ativador de Plasminogênio/genética
Inibidor 1 de Ativador de Plasminogênio/metabolismo
Ligação Proteica/efeitos dos fármacos
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Receptor Tipo 1 de Angiotensina/metabolismo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (Macrolides); 0 (Plasminogen Activator Inhibitor 1); 0 (RNA, Messenger); 0 (Receptor, Angiotensin, Type 1); 11128-99-7 (Angiotensin II); 23025-68-5 (angiotensin II, des-Asp(1)-des-Arg(2)-Ile(5)-); 88899-55-2 (bafilomycin A1); 9088-01-1 (1-Sarcosine-8-Isoleucine Angiotensin II); EC 3.4.11.3 (Cystinyl Aminopeptidase); EC 3.4.11.3 (leucyl-cystinyl aminopeptidase); IY9XDZ35W2 (Glucose); JMS50MPO89 (Losartan)
[Em] Mês de entrada:1012
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100608
[St] Status:MEDLINE
[do] DOI:10.3109/10799893.2010.487491


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Texto completo
[PMID]:20495810
[Au] Autor:Crossley DA; Jonker SS; Hicks JW; Thornburg KL
[Ad] Endereço:Department of Biology, University of North Dakota, 10 Cornell Street, Mail stop 9019, Grand Forks, ND 58202, USA. dane.crossley@und.nodak.edu
[Ti] Título:Maturation of the angiotensin II cardiovascular response in the embryonic White Leghorn chicken (Gallus gallus).
[So] Source:J Comp Physiol B;180(7):1057-65, 2010 Oct.
[Is] ISSN:1432-136X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Angiotensin II (Ang II) is an important regulator of cardiovascular function in adult vertebrates. Although its role in regulating the adult system has been extensively investigated, the cardiovascular response to Ang II in embryonic vertebrates is relatively unknown. We investigated the potential of Ang II as a regulator of cardiovascular function in embryonic chickens, which lack central nervous system control of cardiovascular function throughout the majority of incubation. The cardiovascular response to Ang II in embryonic chickens was investigated over the final 50% of their development. Ang II produced a dose-dependent increase in arterial pressure on each day of development studied, and the response increased in intensity as development progressed. The Ang II type-1 receptor nonspecific competitive peptide antagonist [Sar(1) ile(8)] Ang II blocked the cardiovascular response to subsequent injections of Ang II on day 21 only. The embryonic pressure response to Ang II (hypertension only) differed from that of adult chickens, in which initial hypotension is followed by hypertension. The constant level of gene expression for the Ang II receptor, in conjunction with an increasing pressure response to the peptide, suggests that two Ang II receptor subtypes are present during chicken development. Collectively, the data indicate that Ang II plays an important role in the cardiovascular development of chickens; however, its role in maintaining basal function requires further study.
[Mh] Termos MeSH primário: Angiotensina II/fisiologia
Sistema Cardiovascular/embriologia
Desenvolvimento Embrionário/fisiologia
Receptor Tipo 1 de Angiotensina/metabolismo
Sistema Renina-Angiotensina/fisiologia
[Mh] Termos MeSH secundário: 1-Sarcosina-8-Isoleucina Angiotensina II/farmacologia
Angiotensina II/antagonistas & inibidores
Angiotensina II/sangue
Angiotensina II/farmacologia
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Animais
Pressão Sanguínea/efeitos dos fármacos
Pressão Sanguínea/fisiologia
Sistema Cardiovascular/efeitos dos fármacos
Embrião de Galinha
Membrana Corioalantoide/efeitos dos fármacos
Membrana Corioalantoide/metabolismo
Relação Dose-Resposta a Droga
Regulação da Expressão Gênica no Desenvolvimento/efeitos dos fármacos
Coração/efeitos dos fármacos
Coração/embriologia
Frequência Cardíaca/efeitos dos fármacos
Frequência Cardíaca/fisiologia
Miocárdio/metabolismo
RNA Mensageiro/metabolismo
Receptor Tipo 1 de Angiotensina/genética
Sistema Renina-Angiotensina/efeitos dos fármacos
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (RNA, Messenger); 0 (Receptor, Angiotensin, Type 1); 11128-99-7 (Angiotensin II); 9088-01-1 (1-Sarcosine-8-Isoleucine Angiotensin II)
[Em] Mês de entrada:1101
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100525
[St] Status:MEDLINE
[do] DOI:10.1007/s00360-010-0473-y


  8 / 285 MEDLINE  
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[PMID]:19351865
[Au] Autor:Morinelli TA; Kendall RT; Luttrell LM; Walker LP; Ullian ME
[Ad] Endereço:Division of Nephrology, Department of Medicine, Medical University of South Carolina, Charleston, SC 29425, USA. morinelt@musc.edu
[Ti] Título:Angiotensin II-induced cyclooxygenase 2 expression in rat aorta vascular smooth muscle cells does not require heterotrimeric G protein activation.
[So] Source:J Pharmacol Exp Ther;330(1):118-24, 2009 Jul.
[Is] ISSN:1521-0103
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Angiotensin II (AngII) initiates cellular effects via its G protein-coupled angiotensin 1 (AT(1)) receptor (AT(1)R). Previously, we showed that AngII-induced expression of the prostanoid-producing enzyme cyclooxygenase 2 (COX-2) was dependent upon nuclear trafficking of activated AT(1)R. In the present study, mastoparan (an activator of G proteins), suramin (an inhibitor of G proteins), 1-[6-[[17beta-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione (U73122; a specific inhibitor of phospholipase C), and sarcosine(1)-Ile(4)-Ile(8)-AngII (SII-AngII; a G protein-independent AT(1)R agonist) were used to determine the involvement of G proteins and AT(1A)R trafficking in AngII-stimulated COX-2 protein expression in human embryonic kidney-293 cells stably expressing AT(1A)/green fluorescent protein receptors and cultured vascular smooth muscle cells, respectively. Mastoparan alone stimulated release of intracellular calcium and increased COX-2 expression. Preincubation with mastoparan inhibited AngII-induced calcium signaling without altering AngII-induced AT(1A)R trafficking, p42/44 extracellular signal-regulated kinase (ERK) activation, or COX-2 expression. Suramin or U73122 had no significant effect on their own; they did not inhibit AngII-induced AT(1A)R trafficking, p42/44 ERK activation, or COX-2 expression; but they did inhibit AngII-induced calcium responses. SII-AngII stimulated AT(1A)R trafficking and increased COX-2 protein expression without activating intracellular calcium release. These data suggest that G protein activation results in increased COX-2 protein expression, but AngII-induced COX-2 expression seems to occur independently of G protein activation.
[Mh] Termos MeSH primário: Angiotensina II/fisiologia
Aorta/metabolismo
Ciclo-Oxigenase 2/biossíntese
Proteínas Heterotriméricas de Ligação ao GTP/metabolismo
Músculo Liso Vascular/metabolismo
Miócitos de Músculo Liso/metabolismo
[Mh] Termos MeSH secundário: 1-Sarcosina-8-Isoleucina Angiotensina II/farmacologia
Animais
Aorta/enzimologia
Aorta/fisiologia
Linhagem Celular
Células Cultivadas
Ciclo-Oxigenase 2/genética
Ativação Enzimática/efeitos dos fármacos
Ativação Enzimática/fisiologia
Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos
Regulação Enzimológica da Expressão Gênica/fisiologia
Proteínas Heterotriméricas de Ligação ao GTP/antagonistas & inibidores
Seres Humanos
Músculo Liso Vascular/efeitos dos fármacos
Músculo Liso Vascular/enzimologia
Músculo Liso Vascular/fisiologia
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/enzimologia
Miócitos de Músculo Liso/fisiologia
Peptídeos/farmacologia
Ratos
Venenos de Vespas/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Peptides); 0 (Wasp Venoms); 11128-99-7 (Angiotensin II); 72093-21-1 (mastoparan); 9088-01-1 (1-Sarcosine-8-Isoleucine Angiotensin II); EC 1.14.99.1 (Cyclooxygenase 2); EC 3.6.5.1 (Heterotrimeric GTP-Binding Proteins)
[Em] Mês de entrada:0907
[Cu] Atualização por classe:161025
[Lr] Data última revisão:
161025
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090409
[St] Status:MEDLINE
[do] DOI:10.1124/jpet.109.151829


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[PMID]:19300422
[Au] Autor:Aránguiz-Urroz P; Soto D; Contreras A; Troncoso R; Chiong M; Montenegro J; Venegas D; Smolic C; Ayala P; Thomas WG; Lavandero S; Díaz-Araya G
[Ad] Endereço:Centro FONDAP Estudios Moleculares de la Célula, Facultad Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile.
[Ti] Título:Differential participation of angiotensin II type 1 and 2 receptors in the regulation of cardiac cell death triggered by angiotensin II.
[So] Source:Am J Hypertens;22(5):569-76, 2009 May.
[Is] ISSN:1941-7225
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The Angiotensin II (Ang II) type 1 (AT(1)R) and type 2 (AT(2)R) receptors are increased in the heart following myocardial infarction and dilated cardiomyopathy, yet their contribution at a cellular level to compensation and/or failure remains controversial. METHODS: We ectopically expressed AT(1)R and AT(2)R in cultured adult rat cardiomyocytes and cardiac fibroblasts to investigate Ang II-mediated cardiomyocyte hypertrophy and cardiac cell viability. RESULTS: In adult rat cardiomyocytes, Ang II did not induce hypertrophy via the AT(1)R, and no effect of Ang II on cell viability was observed following AT(1)R or AT(2)R expression. In adult rat cardiac fibroblasts, Ang II stimulated cell death by apoptosis via the AT(1)R (but not the AT(2)R), which required the presence of extracellular calcium, and induced a rapid dissipation of mitochondrial membrane potential, which was significant from 8 h. CONCLUSIONS: We conclude that Ang II/AT(1)R triggers apoptosis in adult rat cardiac fibroblasts, which is dependent on Ca2+ influx.
[Mh] Termos MeSH primário: Angiotensina II/farmacologia
Miócitos Cardíacos/efeitos dos fármacos
Receptor Tipo 1 de Angiotensina/fisiologia
Receptor Tipo 2 de Angiotensina/fisiologia
[Mh] Termos MeSH secundário: 1-Sarcosina-8-Isoleucina Angiotensina II/metabolismo
Adenoviridae/genética
Animais
Apoptose/efeitos dos fármacos
Cálcio/fisiologia
Morte Celular/efeitos dos fármacos
Células Cultivadas
Masculino
Miócitos Cardíacos/metabolismo
Ratos
Ratos Sprague-Dawley
Transdução Genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptor, Angiotensin, Type 1); 0 (Receptor, Angiotensin, Type 2); 11128-99-7 (Angiotensin II); 9088-01-1 (1-Sarcosine-8-Isoleucine Angiotensin II); SY7Q814VUP (Calcium)
[Em] Mês de entrada:0905
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:090321
[St] Status:MEDLINE
[do] DOI:10.1038/ajh.2009.32


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[PMID]:18711690
[Au] Autor:Weiland F; Verspohl EJ
[Ad] Endereço:Department of Pharmacology, Institute of Pharmaceutical and Medicinal Chemistry, University of Münster, Münster, Germany.
[Ti] Título:Variety of angiotensin receptors in 3T3-L1 preadipose cells and differentiated adipocytes.
[So] Source:Horm Metab Res;40(11):760-6, 2008 Nov.
[Is] ISSN:0018-5043
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:A local paracrine acting angiotensin (ANG) system of preadipocytes and mature adipocytes is involved in metabolic effects and tissue differentiation. The present study reports on the investigation of binding affinities for various angiotensin receptors including their relevance in 3T3-L1 adipocytes and preadipocytes and 3T3-442A preadipocytes. Competitive binding studies using both 125I-ANG II and its more stable analogue 125I-SARILE for investigating AT1/AT2 binding sites in 3T3-L1 preadipocytes reveal a biphasic competition curve with KDs at a low and high nanomolar range. By using the AT2 receptor selective ligand 125I-CGP4112A the presence of high affinity AT2 binding sites in preadipocytes was observed. High nonspecific binding and a low receptor number is characteristic for all these experiments. An AT4 binding site (binding site for ANG IV) exists in 3T3-L1 and F442A preadipocytes and adipocytes with a high nanomolar KD. This low binding affinity was confirmed by a biological assay, the IRAP assay (=insulin regulated aminopeptidase assay). IRAP is associated with the AT4 receptor, which is a binding site at the luminal part of membrane bound IRAP. The curves for competition binding and for inhibition of IRAP activity are superimposable with respect to angiotensin IV. In conclusion, AT1 and AT2 binding sites are present in preadipocytes. AT2 receptor binding affinities are shown in preadipocytes for the first time. The description of a non-AT1/AT2 binding site with low affinity remains speculative albeit of high interest because antidiabetic and obesity related effects of angiotensin peptides and sartanes as antagonists are observed at these high concentrations. Local concentrations of ANG II and their degradation products may be extremely high. The low amounts of AT1 and AT2 binding sites emphasize the relevance of other binding sites in adipose tissue development and metabolic effects. The AT4 binding site seems to be one of the predominant receptors in adipose cells. Other degraded, but still bioactive peptides like ANG III, IV and ANG(1-7), activating receptors not influenced by ANG II, could be of importance.
[Mh] Termos MeSH primário: Adipócitos/química
Receptores de Angiotensina/análise
[Mh] Termos MeSH secundário: 1-Sarcosina-8-Isoleucina Angiotensina II/metabolismo
Células 3T3-L1
Adipócitos/citologia
Angiotensina II/metabolismo
Animais
Sítios de Ligação
Ligação Competitiva
Diferenciação Celular
Linhagem Celular
Cistinil Aminopeptidase/metabolismo
Radioisótopos do Iodo
Camundongos
Receptor Tipo 1 de Angiotensina/análise
Receptor Tipo 1 de Angiotensina/metabolismo
Receptor Tipo 2 de Angiotensina/análise
Receptor Tipo 2 de Angiotensina/metabolismo
Receptores de Angiotensina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AT4 receptor); 0 (Iodine Radioisotopes); 0 (Receptor, Angiotensin, Type 1); 0 (Receptor, Angiotensin, Type 2); 0 (Receptors, Angiotensin); 11128-99-7 (Angiotensin II); 9088-01-1 (1-Sarcosine-8-Isoleucine Angiotensin II); EC 3.4.11.3 (Cystinyl Aminopeptidase); EC 3.4.11.3 (leucyl-cystinyl aminopeptidase)
[Em] Mês de entrada:0902
[Cu] Atualização por classe:090219
[Lr] Data última revisão:
090219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:080820
[St] Status:MEDLINE
[do] DOI:10.1055/s-0028-1082041



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