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[PMID]:25403411
[Au] Autor:Spasov AA; Yakovlev DS; Bukatina TM; Brigadirova AA
[Ad] Endereço:Volgograd State Medical University, Ministry of Health of the Russian Federation; Volgograd Medical Scientific Center, Volgograd, Russia.
[Ti] Título:In vitro method of studying the angiotensin activity of chemical compounds.
[So] Source:Bull Exp Biol Med;158(1):115-7, 2014 Nov.
[Is] ISSN:1573-8221
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We developed and tested an experimental model to study in vitro the type 1 angiotensin antagonistic activity of compounds on the isolated portal vein of rats. The reliability of this method was confirmed in tests with saralasin (nonselective antagonist of angiotensin receptors) and losartan (selective antagonist of type 1 angiotensin receptors) in concentrations of 10(-9)-10(-5) mol/liter. The half-maximal inhibitory concentrations (IC50) of these substances were calculated.
[Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Losartan/farmacologia
Saralasina/farmacologia
[Mh] Termos MeSH secundário: Animais
Avaliação Pré-Clínica de Medicamentos
Feminino
Técnicas In Vitro
Concentração Inibidora 50
Masculino
Contração Muscular/efeitos dos fármacos
Músculo Liso Vascular/efeitos dos fármacos
Veia Porta/efeitos dos fármacos
Veia Porta/fisiologia
Ratos Wistar
Vasoconstrição/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); H2AFV2HE66 (Saralasin); JMS50MPO89 (Losartan)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:141125
[Lr] Data última revisão:
141125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141119
[St] Status:MEDLINE
[do] DOI:10.1007/s10517-014-2705-8


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[PMID]:23219939
[Au] Autor:Guethe LM; Pelegrini-da-Silva A; Borelli KG; Juliano MA; Pelosi GG; Pesquero JB; Silva CL; Corrêa FM; Murad F; Prado WA; Martins AR
[Ad] Endereço:Department of Psychology, FFCLRP University of São Paulo, Ribeirão Preto 14049-901, SP, Brazil.
[Ti] Título:Angiotensin (5-8) modulates nociception at the rat periaqueductal gray via the NO-sGC pathway and an endogenous opioid.
[So] Source:Neuroscience;231:315-27, 2013 Feb 12.
[Is] ISSN:1873-7544
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Angiotensins (Angs) modulate blood pressure, hydro-electrolyte composition, and antinociception. Although Ang (5-8) has generally been considered to be inactive, we show here that Ang (5-8) was the smallest Ang to elicit dose-dependent responses and receptor-mediated antinociception in the rat ventrolateral periaqueductal gray matter (vlPAG). Ang (5-8) antinociception seems to be selective, because it did not alter blood pressure or act on vascular or intestinal smooth muscle cells. The non-selective Ang-receptor (Ang-R) antagonist saralasin blocked Ang (5-8) antinociception, but selective antagonists of Ang-R types I, II, IV, and Mas did not, suggesting that Ang (5-8) may act via an unknown receptor. Endopeptidase EP 24.11 and amastatin-sensitive aminopeptidase from the vlPAG catalyzed the synthesis (from Ang II or Ang III) and inactivation of Ang (5-8), respectively. Selective inhibitors of neuronal-nitric oxide (NO) synthase, soluble guanylyl cyclase (sGC) and a non-selective opioid receptor (opioid-R) inhibitor blocked Ang (5-8)-induced antinociception. In conclusion, Ang (5-8) is a new member of the Ang family that selectively and strongly modulates antinociception via NO-sGC and endogenous opioid in the vlPAG.
[Mh] Termos MeSH primário: Angiotensina I/farmacologia
Guanilato Ciclase/metabolismo
Óxido Nítrico/metabolismo
Nociceptividade/efeitos dos fármacos
Peptídeos Opioides/metabolismo
Fragmentos de Peptídeos/farmacologia
Substância Cinzenta Periaquedutal/efeitos dos fármacos
Receptores Citoplasmáticos e Nucleares/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Antagonistas de Receptores de Angiotensina/farmacologia
Animais
Aorta/efeitos dos fármacos
Relação Dose-Resposta a Droga
Frequência Cardíaca/fisiologia
Masculino
Contração Muscular/efeitos dos fármacos
Músculo Liso/efeitos dos fármacos
Peptídeos Opioides/antagonistas & inibidores
Ratos
Ratos Wistar
Saralasina/farmacologia
Guanilil Ciclase Solúvel
Teprotida/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiotensin Receptor Antagonists); 0 (Opioid Peptides); 0 (Peptide Fragments); 0 (Receptors, Cytoplasmic and Nuclear); 31C4KY9ESH (Nitric Oxide); 9041-90-1 (Angiotensin I); C3E5QBF1R6 (Teprotide); EC 4.6.1.2 (Guanylate Cyclase); EC 4.6.1.2 (Soluble Guanylyl Cyclase); H2AFV2HE66 (Saralasin)
[Em] Mês de entrada:1307
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:121211
[St] Status:MEDLINE


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[PMID]:22535800
[Au] Autor:Zhang J; Wu J; Gu C; Noble NA; Border WA; Huang Y
[Ad] Endereço:Fibrosis Research Laboratory, Division of Nephrology and Hypertension, Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City, USA.
[Ti] Título:Receptor-mediated nonproteolytic activation of prorenin and induction of TGF-ß1 and PAI-1 expression in renal mesangial cells.
[So] Source:Am J Physiol Renal Physiol;303(1):F11-20, 2012 Jul 01.
[Is] ISSN:1522-1466
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:While elevated plasma prorenin levels are commonly found in diabetic patients and correlate with diabetic nephropathy, the pathological role of prorenin, if any, remains unclear. Prorenin binding to the (pro)renin receptor [(p)RR] unmasks prorenin catalytic activity. We asked whether elevated prorenin could be activated at the site of renal mesangial cells (MCs) through receptor binding without being proteolytically converted to renin. Recombinant inactive rat prorenin and a mutant prorenin that is noncleavable, i.e., cannot be activated proteolytically, are produced in 293 cells. After MCs were incubated with 10(-7) M native or mutant prorenin for 6 h, cultured supernatant acquired the ability to generate angiotensin I (ANG I) from angiotensinogen, indicating both prorenins were activated. Small interfering RNA (siRNA) against the (p)RR blocked their activation. Furthermore, either native or mutant rat prorenin at 10(-7) M alone similarly and significantly induced transforming growth factor-ß(1), plasminogen activator inhibitor-1 (PAI-1), and fibronectin mRNA expression, and these effects were blocked by (p)RR siRNA, but not by the ANG II receptor antagonist, saralasin. When angiotensinogen was also added to cultured MCs with inactive native or mutant prorenin, PAI-1 and fibronectin were further increased significantly compared with prorenin or mutant prorenin alone. This effect was blocked partially by treatment with (p)RR siRNA or saralasin. We conclude that prorenin binds the (p)RR on renal MCs and is activated nonproteolytically. This activation leads to increased expression of PAI-1 and transforming growth factor-ß(1) via ANG II-independent and ANG II-dependent mechanisms. These data provide a mechanism by which elevated prorenin levels in diabetes may play a role in the development of diabetic nephropathy.
[Mh] Termos MeSH primário: Angiotensina I/metabolismo
Células Mesangiais/metabolismo
Inibidor 1 de Ativador de Plasminogênio/metabolismo
Renina/farmacologia
Fator de Crescimento Transformador beta1/metabolismo
[Mh] Termos MeSH secundário: Inibidores da Enzima Conversora de Angiotensina/farmacologia
Animais
Células Cultivadas
Fibronectinas/genética
Fibronectinas/metabolismo
Masculino
Células Mesangiais/citologia
Células Mesangiais/efeitos dos fármacos
Inibidor 1 de Ativador de Plasminogênio/genética
Ratos
Ratos Sprague-Dawley
Saralasina/farmacologia
Fator de Crescimento Transformador beta1/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Fibronectins); 0 (Plasminogen Activator Inhibitor 1); 0 (Transforming Growth Factor beta1); 9041-90-1 (Angiotensin I); EC 3.4.23.15 (Renin); H2AFV2HE66 (Saralasin)
[Em] Mês de entrada:1209
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120427
[St] Status:MEDLINE
[do] DOI:10.1152/ajprenal.00050.2012


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[PMID]:22116365
[Au] Autor:Wagner CA; Mohebbi N; Uhlig U; Giebisch GH; Breton S; Brown D; Geibel JP
[Ad] Endereço:Department of Cellular and Molecular Physiology, School of Medicine, Yale University, New Haven, CT, USA. Wagnerca@access.uzh.ch
[Ti] Título:Angiotensin II stimulates H⁺-ATPase activity in intercalated cells from isolated mouse connecting tubules and cortical collecting ducts.
[So] Source:Cell Physiol Biochem;28(3):513-20, 2011.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Intercalated cells in the collecting duct system express V-type H(+)-ATPases which participate in acid extrusion, bicarbonate secretion, and chloride absorption depending on the specific subtype. The activity of H(+)-ATPases is regulated by acid-base status and several hormones, including angiotensin II and aldosterone. Angiotensin II stimulates chloride absorption mediated by pendrin in type B intercalated cells and this process is energized by the activity of H(+)-ATPases. Moreover, angiotensin II stimulates bicarbonate secretion by the connecting tubule (CNT) and early cortical collecting duct (CCD). In the present study we examined the effect of angiotensin II (10 nM) on H(+)-ATPase activity and localization in isolated mouse connecting tubules and cortical collecting ducts. Angiotensin II stimulated Na(+)-independent intracellular pH recovery about 2-3 fold, and this was abolished by the specific H(+)-ATPase inhibitor concanamycin. The effect of angiotensin II was mediated through type 1 angiotensin II receptors (AT(1)-receptors) because it could be blocked by saralasin. Stimulation of H(+)-ATPase activity required an intact microtubular network--it was completely inhibited by colchicine. Immunocytochemistry of isolated CNT/CCDs incubated in vitro with angiotensin II suggests enhanced membrane associated staining of H(+)-ATPases in pendrin expressing intercalated cells. In summary, angiotensin II stimulates H(+)-ATPases in CNT/CCD intercalated cells, and may contribute to the regulation of chloride absorption and bicarbonate secretion in this nephron segment.
[Mh] Termos MeSH primário: Angiotensina II/farmacologia
Córtex Renal/enzimologia
Túbulos Renais Coletores/enzimologia
ATPases Vacuolares Próton-Translocadoras/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas de Transporte de Ânions/metabolismo
Bicarbonatos/metabolismo
Membrana Celular/metabolismo
Cloretos/metabolismo
Colchicina/farmacologia
Concentração de Íons de Hidrogênio
Imuno-Histoquímica
Córtex Renal/citologia
Córtex Renal/patologia
Túbulos Renais Coletores/citologia
Túbulos Renais Coletores/patologia
Macrolídeos/farmacologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Receptores de Angiotensina/química
Receptores de Angiotensina/metabolismo
Saralasina/farmacologia
Sódio/metabolismo
ATPases Vacuolares Próton-Translocadoras/análise
ATPases Vacuolares Próton-Translocadoras/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anion Transport Proteins); 0 (Bicarbonates); 0 (Chlorides); 0 (Macrolides); 0 (Receptors, Angiotensin); 0 (Slc26a4 protein, mouse); 11128-99-7 (Angiotensin II); 80890-47-7 (concanamycin A); 9NEZ333N27 (Sodium); EC 3.6.1.- (Vacuolar Proton-Translocating ATPases); H2AFV2HE66 (Saralasin); SML2Y3J35T (Colchicine)
[Em] Mês de entrada:1203
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111126
[St] Status:MEDLINE
[do] DOI:10.1159/000335112


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[PMID]:22009728
[Au] Autor:Ferreira R; Gasperin B; Rovani M; Santos J; Barreta M; Bohrer R; Price C; Gonçalves PB
[Ad] Endereço:Laboratório de Biotecnologia e Reprodução Animal, Universidade Federal de Santa Maria, Santa Maria, Brazil.
[Ti] Título:Angiotensin II signaling promotes follicle growth and dominance in cattle.
[So] Source:Endocrinology;152(12):4957-65, 2011 Dec.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:It is generally understood that angiotensin II (AngII) promotes follicle atresia in rats, although recent data suggested that this may not be true in cattle. In this study, we aimed to determine in vivo whether AngII alters follicle development in cattle, using intrafollicular injection of AngII or antagonist into the growing dominant follicle or the second largest subordinate follicle. Injection of saralasin, an AngII antagonist, into the growing dominant follicle inhibited follicular growth, and this inhibitory effect was overcome by systemic FSH supplementation. Injection of AngII into the dominant follicle did not affect follicular growth, whereas injection of AngII into the second largest follicle prevented the expected atresia of this subordinate follicle, and the treated follicle grew at the same rate as the dominant follicle for the next 24 h. Inhibition of AngII action in the dominant follicle decreased estradiol concentrations in follicular fluid and the abundance of mRNA encoding aromatase, 3ß-hydroxysteroid dehydrogenase, LH receptor, and cyclinD2 in granulosa cells, with minimal effects on theca cells. The effect of AngII on aromatase mRNA levels was confirmed using an in vitro granulosa cell culture system. In conclusion, these data suggest that AngII signaling promotes follicle growth in cattle and does so by regulating genes involved in estradiol secretion and granulosa cell proliferation and differentiation.
[Mh] Termos MeSH primário: Angiotensina II/farmacologia
Folículo Ovariano/crescimento & desenvolvimento
Transdução de Sinais
[Mh] Termos MeSH secundário: Angiotensina II/administração & dosagem
Angiotensina II/fisiologia
Bloqueadores do Receptor Tipo 1 de Angiotensina II
Animais
Aromatase
Bovinos
Diferenciação Celular
Proliferação Celular
Estradiol
Feminino
Regulação da Expressão Gênica
Células da Granulosa/citologia
Células da Granulosa/efeitos dos fármacos
Folículo Ovariano/efeitos dos fármacos
Saralasina/administração & dosagem
Saralasina/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 11128-99-7 (Angiotensin II); 4TI98Z838E (Estradiol); EC 1.14.14.1 (Aromatase); H2AFV2HE66 (Saralasin)
[Em] Mês de entrada:1202
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:111020
[St] Status:MEDLINE
[do] DOI:10.1210/en.2011-1146


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[PMID]:21613610
[Au] Autor:Deliu E; Tica AA; Motoc D; Brailoiu GC; Brailoiu E
[Ad] Endereço:Department of Pharmacology, Temple University School of Medicine, Philadelphia, Pennslyvania 19140, USA.
[Ti] Título:Intracellular angiotensin II activates rat myometrium.
[So] Source:Am J Physiol Cell Physiol;301(3):C559-65, 2011 Sep.
[Is] ISSN:1522-1563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Angiotensin II is a modulator of myometrial activity; both AT(1) and AT(2) receptors are expressed in myometrium. Since in other tissues angiotensin II has been reported to activate intracellular receptors, we assessed the effects of intracellular administration of angiotensin II via microinjection on myometrium, using calcium imaging. Intracellular injection of angiotensin II increased cytosolic Ca(2+) concentration ([Ca(2+)](i)) in myometrial cells in a dose-dependent manner. The effect was abolished by the AT(1) receptor antagonist losartan but not by the AT(2) receptor antagonist PD-123319. Disruption of the endo-lysosomal system, but not that of Golgi apparatus, prevented the angiotensin II-induced increase in [Ca(2+)](i). Blockade of AT(1) receptor internalization had no effect, whereas blockade of microautophagy abolished the increase in [Ca(2+)](i) produced by intracellular injection of angiotensin II; this indicates that microautophagy is a critical step in transporting the peptide into the endo-lysosomes lumenum. The response to angiotensin II was slightly reduced in Ca(2+)-free saline, indicating a major involvement of Ca(2+) release from internal stores. Blockade of inositol 1,4,5-trisphosphate (IP(3)) receptors with heparin and xestospongin C or inhibition of phospholipase C (PLC) with U-73122 abolished the response to angiotensin II, supporting the involvement of PLC-IP(3) pathway. Angiotensin II-induced increase in [Ca(2+)](i) was slightly reduced by antagonism of ryanodine receptors. Taken together, our results indicate for the first time that in myometrial cells, intracellular angiotensin II activates AT(1)-like receptors on lysosomes and activates PLC-IP(3)-dependent Ca(2+) release from endoplasmic reticulum; the response is further augmented by a Ca(2+)-induced Ca(2+) release mechanism via ryanodine receptors activation.
[Mh] Termos MeSH primário: Angiotensina II/metabolismo
Sinalização do Cálcio/fisiologia
Miométrio/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Angiotensina II/administração & dosagem
Angiotensina II/farmacologia
Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Bloqueadores do Receptor Tipo 2 de Angiotensina II/farmacologia
Animais
Arsenicais/farmacologia
Autofagia/efeitos dos fármacos
Brefeldina A/farmacologia
Sinalização do Cálcio/efeitos dos fármacos
Carbolinas/farmacologia
Células Cultivadas
Ácido Egtázico/farmacologia
Endocitose/efeitos dos fármacos
Retículo Endoplasmático/efeitos dos fármacos
Retículo Endoplasmático/metabolismo
Endossomos/metabolismo
Inibidores Enzimáticos/farmacologia
Estrenos/farmacologia
Feminino
Heparina/farmacologia
Imidazóis/administração & dosagem
Imidazóis/farmacologia
Receptores de Inositol 1,4,5-Trifosfato/antagonistas & inibidores
Receptores de Inositol 1,4,5-Trifosfato/metabolismo
Losartan/administração & dosagem
Losartan/farmacologia
Lisossomos/metabolismo
Compostos Macrocíclicos/farmacologia
Macrolídeos/farmacologia
Modelos Biológicos
Miométrio/citologia
Miométrio/efeitos dos fármacos
NADP/análogos & derivados
NADP/metabolismo
Oxazóis/farmacologia
Piperazinas/farmacologia
Piridinas/administração & dosagem
Piridinas/farmacologia
Pirrolidinonas/farmacologia
Ratos
Ratos Sprague-Dawley
Receptor Tipo 1 de Angiotensina/metabolismo
Receptor Tipo 2 de Angiotensina/metabolismo
Rianodina/farmacologia
Saralasina/administração & dosagem
Saralasina/farmacologia
Transdução de Sinais/efeitos dos fármacos
Sirolimo/farmacologia
Fosfolipases Tipo C/antagonistas & inibidores
Fosfolipases Tipo C/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (1-(3-((4-(2-fluorophenyl)piperazin-1-yl)methyl)-4-methoxyphenyl)-2,3,4,9-tetrahydro-1H-pyrido(3,4-b)indole-3-carboxylic acid); 0 (Angiotensin II Type 1 Receptor Blockers); 0 (Angiotensin II Type 2 Receptor Blockers); 0 (Arsenicals); 0 (Carbolines); 0 (Enzyme Inhibitors); 0 (Estrenes); 0 (Imidazoles); 0 (Inositol 1,4,5-Trisphosphate Receptors); 0 (Macrocyclic Compounds); 0 (Macrolides); 0 (Oxazoles); 0 (Piperazines); 0 (Pyridines); 0 (Pyrrolidinones); 0 (Receptor, Angiotensin, Type 1); 0 (Receptor, Angiotensin, Type 2); 0 (xestospongin C); 0HUR2WY345 (oxophenylarsine); 11128-99-7 (Angiotensin II); 112648-68-7 (1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione); 130663-39-7 (PD 123319); 15662-33-6 (Ryanodine); 20350-15-6 (Brefeldin A); 526U7A2651 (Egtazic Acid); 53-59-8 (NADP); 5502-96-5 (NAADP); 88899-55-2 (bafilomycin A1); 9005-49-6 (Heparin); EC 3.1.4.- (Type C Phospholipases); H2AFV2HE66 (Saralasin); JMS50MPO89 (Losartan); W36ZG6FT64 (Sirolimus)
[Em] Mês de entrada:1201
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110527
[St] Status:MEDLINE
[do] DOI:10.1152/ajpcell.00123.2011


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[PMID]:20828629
[Au] Autor:Frenkel L; Suárez LD; Maldonado H; Delorenzi A
[Ad] Endereço:Laboratorio de Neurobiología de la Memoria, Departamento de Fisiología y Biología Molecular, IFIByNE-CONICET, Pabellón II, FCEyN, Universidad de Buenos Aires, Ciudad Universitaria (C1428EHA), Argentina. frenkel@leloir.org.ar
[Ti] Título:Angiotensin modulates long-term memory expression but not long-term memory storage in the crab Chasmagnathus.
[So] Source:Neurobiol Learn Mem;94(4):509-20, 2010 Nov.
[Is] ISSN:1095-9564
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Memory reconsolidation is a dynamic process in which a previously consolidated memory becomes labile following reactivation by a reminder. In a previous study in the crab Chasmagnathus memory model, we showed that a water-shortage episode, via angiotensin modulation during reconsolidation, could reveal a memory that otherwise remains unexpressed: weakly trained animals cannot reveal long-term memory (LTM) except when an episode of noticeable ethological meaning, water deprivation, is contingent upon reconsolidation. However, these results are at variance with two of our previous interpretations: weak training protocols do not build LTM and angiotensin II modulates the strength of the information storing process. A parsimonious hypothesis is that in Chasmagnathus angiotensins regulate LTM expression, but not LTM storage. Here, we tested three predictions of this hypothesis. First, the well-known retrograde amnesic effect of the angiotensin II antagonist saralasin is not due to interference on memory storage, but to modulation of memory expression. Second, the recovery of the LTM memory expression of the apparently amnesic retrograde effect produced by saralasin, through the water-shortage episode contingent upon reconsolidation, must be reconsolidation specific. Consequently, summation-like effects and retrieval deficits cannot explain these results because of the parametric conditions of reconsolidation. Third, weak training protocols build an unexpressed LTM that requires mRNA transcription and translation, a diagnostic characteristic of LTM. Results show that angiotensin modulates LTM expression but not LTM memory storage in the crab Chasmagnathus. The results lead us to suggest that, in Chasmagnathus, LTM expression - the process of gaining appreciable control over behavior of the reactivated trace in the retrieval session - may be considered a distinct attribute of its long-term storage. This strategy, a positive modulation during reconsolidation, is proposed to distinguish between memories that can be reactivated, labilized and are not expressed, and memories that are not stored long term, obliterated or altered in other retrieval mechanisms.
[Mh] Termos MeSH primário: Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia
Angiotensina II/fisiologia
Braquiúros/fisiologia
Memória de Longo Prazo/fisiologia
Saralasina/farmacologia
[Mh] Termos MeSH secundário: Animais
Aprendizagem por Associação/efeitos dos fármacos
Aprendizagem por Associação/fisiologia
Meio Ambiente
Masculino
Memória de Longo Prazo/efeitos dos fármacos
Rememoração Mental/efeitos dos fármacos
Rememoração Mental/fisiologia
Recognição (Psicologia)/efeitos dos fármacos
Recognição (Psicologia)/fisiologia
Privação de Água/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); 11128-99-7 (Angiotensin II); H2AFV2HE66 (Saralasin)
[Em] Mês de entrada:1102
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100911
[St] Status:MEDLINE
[do] DOI:10.1016/j.nlm.2010.09.003


  8 / 1480 MEDLINE  
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[PMID]:20429803
[Au] Autor:Varoni MV; Palomba D; Macciotta NP; Antuofermo E; Deiana G; Baralla E; Anania V; Demontis MP
[Ad] Endereço:Department of Animal Biology, Division of Pharmacology, University of Sassari, Sassari, Italy. varoni@uniss.it
[Ti] Título:Brain renin-angiotensin system modifies the blood pressure response to intracerebroventricular cadmium in rats.
[So] Source:Drug Chem Toxicol;33(3):302-9, 2010 Jul.
[Is] ISSN:1525-6014
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In order to elucidate the involvement of the brain renin-angiotensin system (RAS) in cadmium intracerebroventricular (ICV) hypertension, we evaluated the effects of a pretreatment with different drugs: clonidine, an alpha(2) adrenergic agonist, enalapril and captopril, both ACE inhibitors, and saralasin, a competitive nonselective AT(1) and AT(2) receptor antagonist. We used a rat strain with low levels of kallikrein (LKR) that was more sensitive to ICV cadmium hypertension, compared with normal kallikrein rats (NKRs), the control strain. The interplay between the kallikrein-kinin system and the RAS in the LKR strain caused various hemodynamic alterations, which we believe were the result of elevated RAS activity in these animals. Moreover, we suggest that the defective kallikrein-kinin system in LKR may also cause an alteration in the activation of brain RAS in these animals. The LKR displayed elevated concentrations of plasma AII, hypertrophy of the myocardium, and initial alterations in the renal glomerulotubular system. With the exception of clonidine, all of the other drugs showed greater antihypertensive effects of differing statistical significance in LKR, compared with NKR. Both ACE inhibitors were able to significantly reduce pressor response to cadmium ICV in LKR throughout the experiment, whereas in NKR, they were only able to reduce the hypertensive peak of cadmium. A significant protective effect was also observed in LKR pretreated with saralasin, while no effect was observed in NKR. These findings confirm the presence of brain RAS activation in LKR and its contribution to the central control of pressor response to cadmium ICV.
[Mh] Termos MeSH primário: Encéfalo/fisiologia
Cádmio/toxicidade
Hipertensão/induzido quimicamente
Sistema Calicreína-Cinina/efeitos dos fármacos
Sistema Renina-Angiotensina/fisiologia
[Mh] Termos MeSH secundário: Agonistas alfa-Adrenérgicos/farmacologia
Angiotensina II/sangue
Inibidores da Enzima Conversora de Angiotensina/farmacologia
Animais
Captopril/farmacologia
Clonidina/farmacologia
Enalapril/farmacologia
Coração/fisiopatologia
Histocitoquímica
Hipertensão/fisiopatologia
Sistema Calicreína-Cinina/fisiologia
Calicreínas/urina
Rim/fisiopatologia
Masculino
Ratos
Ratos Wistar
Saralasina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic alpha-Agonists); 0 (Angiotensin-Converting Enzyme Inhibitors); 00BH33GNGH (Cadmium); 11128-99-7 (Angiotensin II); 69PN84IO1A (Enalapril); 9G64RSX1XD (Captopril); EC 3.4.21.- (Kallikreins); H2AFV2HE66 (Saralasin); MN3L5RMN02 (Clonidine)
[Em] Mês de entrada:1009
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:100501
[St] Status:MEDLINE
[do] DOI:10.3109/01480540903418496


  9 / 1480 MEDLINE  
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[PMID]:20035857
[Au] Autor:Tung JN; Lang YD; Wang LF; Chen CM
[Ad] Endereço:Department of Surgery, Tungs' Taichung MetroHarbor Hospital, Taichung, Taiwan.
[Ti] Título:Paraquat increases connective tissue growth factor and collagen expression via angiotensin signaling pathway in human lung fibroblasts.
[So] Source:Toxicol In Vitro;24(3):803-8, 2010 Apr.
[Is] ISSN:1879-3177
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Survivors of paraquat poisoning are left with pulmonary fibrosis which results in a restrictive type of long-term pulmonary dysfunction. Connective tissue growth factor (CTGF) is a key growth factor that initiates tissue repair and underlies the development of lung fibrosis. Angiotensin (ANG) II may induce CTGF expression in the heart and kidney and plays an important role in the pathogenesis of lung fibrosis. The biological effects of ANG II are mediated by ANG II type 1 receptor (AT1R) and AT2R. The aims of this study were to investigate the effects of paraquat on ANG II, ANG II receptors, CTGF, and collagen expressions and to assess the role of ANG II receptors in paraquat-induced collagen synthesis in human lung fibroblasts (MRC-5). MRC-5 cells were incubated with various concentrations of paraquat with or without the ANG II receptor antagonist, saralasin. Paraquat increased ANG II production and AT1R mRNA and protein expression and decreased AT2R mRNA expression. Furthermore, paraquat treatment increased CTGF and collagen mRNA and protein expression in a dose-dependent manner and saralasin inhibited these effects. These results indicate that paraquat increases CTGF and collagen expression by activating angiotensin signaling pathway in human lung fibroblasts.
[Mh] Termos MeSH primário: Angiotensina II/fisiologia
Colágeno/biossíntese
Fator de Crescimento do Tecido Conjuntivo/metabolismo
Fibroblastos/efeitos dos fármacos
Herbicidas/toxicidade
Paraquat/toxicidade
[Mh] Termos MeSH secundário: Inibidores da Enzima Conversora de Angiotensina/farmacologia
Western Blotting
Colágeno Tipo I/biossíntese
Colágeno Tipo II/biossíntese
Relação Dose-Resposta a Droga
Imunofluorescência
Herbicidas/antagonistas & inibidores
Seres Humanos
Paraquat/antagonistas & inibidores
RNA Mensageiro/biossíntese
RNA Mensageiro/genética
Receptor Tipo 2 de Angiotensina/biossíntese
Receptor Tipo 2 de Angiotensina/genética
Receptores de Angiotensina/efeitos dos fármacos
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Saralasina/farmacologia
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Collagen Type I); 0 (Collagen Type II); 0 (Herbicides); 0 (RNA, Messenger); 0 (Receptor, Angiotensin, Type 2); 0 (Receptors, Angiotensin); 11128-99-7 (Angiotensin II); 139568-91-5 (Connective Tissue Growth Factor); 9007-34-5 (Collagen); H2AFV2HE66 (Saralasin); PLG39H7695 (Paraquat)
[Em] Mês de entrada:1006
[Cu] Atualização por classe:141120
[Lr] Data última revisão:
141120
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:091229
[St] Status:MEDLINE
[do] DOI:10.1016/j.tiv.2009.12.015


  10 / 1480 MEDLINE  
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[PMID]:19942847
[Au] Autor:Grothusen A; Divchev D; Luchtefeld M; Schieffer B
[Ad] Endereço:Department of Cardiology and Angiology, Medical School of Hannover, Hannover, Germany.
[Ti] Título:Angiotensin II type 1 receptor blockade: high hopes sent back to reality?
[So] Source:Minerva Cardioangiol;57(6):773-85, 2009 Dec.
[Is] ISSN:0026-4725
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Chronic activation of the renin-angiotensin system (RAS) plays a crucial role in the development of various cardiovascular diseases (CVD). Thus, effective RAS inhibition has been a major achievement to improve the treatment of patients at risk for CVDs, such as myocardial infarction, heart failure and stroke. Three substance classes that block RAS-activation are currently available, angiotensin converting enzyme (ACE) inhibitors, angiotensin II type 1 receptor blockade (ARB) and renin inhibitors. Although the overall goal of these drugs remains the blockade of RAS activation, their individual targets in this system vary and may substantially influence the clinical benefit derived from the long term use of these substances. Here, we summarize the evidence available for the use of ARBs in different cardiovascular pathologies and the impact of this evidence on current treatment guidelines for patients at risk for CVD. Today, ARBs represent a good alternative in case of ACE-inhibitor intolerance due to their outstanding tolerability. ARBs in comparison to ACE-inhibitors have been proven to exert similar effective in the treatment of systolic heart failure, primary prevention of stroke, new onset of diabetes mellitus (DM) type 2 and DM type 2 dependent macroalbuminuria. ARBs should be considered as alternatives to ACE-inhibitors in subjects post-myocardial infarction. Overall however, there is no profound proof for a specific cardiovascular protection by blockade of the angiotensin II Type 1 (AT1) receptor that exceeds the impact of ACE-inhibition or synergises with ACE-blockade. In fact, combination of ARBs and ACE-inhibitor result in an increased rate of adverse effects and, therefore, this combination should not be encouraged. To summarize, the initial hope for a more specific impact on cardiovascular diseases by inhibition of the AT1-receptor in comparison to ACE-inhibition has not come true. However, ARBs have been proven to be equally effective as ACE-blockade in a large variety of clinical settings.
[Mh] Termos MeSH primário: Doenças Cardiovasculares/epidemiologia
Hipertensão/tratamento farmacológico
[Mh] Termos MeSH secundário: Anlodipino/administração & dosagem
Bloqueadores do Receptor Tipo 1 de Angiotensina II/administração & dosagem
Bloqueadores do Receptor Tipo 1 de Angiotensina II/uso terapêutico
Inibidores da Enzima Conversora de Angiotensina/administração & dosagem
Inibidores da Enzima Conversora de Angiotensina/efeitos adversos
Inibidores da Enzima Conversora de Angiotensina/uso terapêutico
Anti-Hipertensivos/administração & dosagem
Anti-Hipertensivos/uso terapêutico
Bloqueadores dos Canais de Cálcio/administração & dosagem
Bloqueadores dos Canais de Cálcio/uso terapêutico
Doenças Cardiovasculares/mortalidade
Doenças Cardiovasculares/prevenção & controle
Consenso
Diabetes Mellitus Tipo 2/tratamento farmacológico
Quimioterapia Combinada
Seguimentos
Insuficiência Cardíaca/tratamento farmacológico
Hospitalização
Seres Humanos
Hipertensão/mortalidade
Hipertrofia Ventricular Esquerda/tratamento farmacológico
Meia-Idade
Guias de Prática Clínica como Assunto
Prevenção Primária
Ensaios Clínicos Controlados Aleatórios como Assunto
Sistema Renina-Angiotensina/efeitos dos fármacos
Sistema Renina-Angiotensina/fisiologia
Fatores de Risco
Saralasina/administração & dosagem
Saralasina/uso terapêutico
Prevenção Secundária
Acidente Vascular Cerebral/prevenção & controle
Tetrazóis/administração & dosagem
Tetrazóis/uso terapêutico
Fatores de Tempo
Resultado do Tratamento
Valina/administração & dosagem
Valina/análogos & derivados
Valina/uso terapêutico
Valsartana
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Angiotensin II Type 1 Receptor Blockers); 0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Antihypertensive Agents); 0 (Calcium Channel Blockers); 0 (Tetrazoles); 1J444QC288 (Amlodipine); 80M03YXJ7I (Valsartan); H2AFV2HE66 (Saralasin); HG18B9YRS7 (Valine)
[Em] Mês de entrada:1004
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:091128
[St] Status:MEDLINE



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