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[PMID]:29314204
[Au] Autor:Jin Z; Tan Q; Sun B
[Ad] Endereço:State Key Laboratory of Biomembrane and Membrane Biotechnology, School of Medicine, Tsinghua University, Beijing, China.
[Ti] Título:Telmisartan ameliorates vascular endothelial dysfunction in coronary slow flow phenomenon (CSFP).
[So] Source:Cell Biochem Funct;36(1):18-26, 2018 Jan.
[Is] ISSN:1099-0844
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Coronary slow flow phenomenon (CSFP) is a coronary microvascular disorder with an increasing morbidity, and currently, available therapies are of limited clinical value for its cure. Hence, it is urgent to find a novel approach to CSFP treatment. Several studies show that endothelial dysfunction plays a critical role in the aetiology of CSFP. Telmisartan (TMST) is a clinically available anti-hypertensive medicine and has shown its potential properties for improving vascular endothelial function. Thus, we aimed to investigate the effect of TMST on endothelial dysfunction in CSFP, Endothelial-dependent flow-mediated vasodilation, serum levels of nitric oxide, adiponectin, and endothelin-1 were surveyed before and after 3 months of TMST treatment. And the percentages of vasodilator response to acetylcholine (Ach) were detected after 12 weeks of TMST treatment. Compare with pretreatment, flow-mediated vasodilation, nitric oxide, and adiponectin were substantially improved after TMST treatment; meanwhile, endothelin-1 was decreased in the TMST group (all P < .01). Compared with the model group, the vasodilator response to Ach was enormously increased after TMST intervention. Additionally, administration of SU11274 or GW9662 would partially reverse the protective effects of TMST on accumulative concentration-vasodilator responses to Ach (P < .01). We demonstrated that administration of TMST could remarkably increase the mRNA and/or protein levels of hepatocyte growth factor, mesenchymal-epithelial transition factor, peroxisome proliferation-activated receptor γ, whereas dramatically diminish mRNA and/or protein levels of p-JNK1/2, mitogen-activated protein kinase, and nuclear factor kappa B (P < .05). Our results thus implicate that TMST ameliorates endothelial dysfunction in CSFP. It is suggested that TSMF may play an important role in the medication of CSFP.
[Mh] Termos MeSH primário: Benzimidazóis/farmacologia
Benzimidazóis/uso terapêutico
Benzoatos/farmacologia
Benzoatos/uso terapêutico
Endotélio Vascular/efeitos dos fármacos
Endotélio Vascular/fisiopatologia
Fenômeno de não Refluxo/tratamento farmacológico
[Mh] Termos MeSH secundário: Angiotensina II/farmacologia
Animais
Benzimidazóis/química
Benzoatos/química
Relação Dose-Resposta a Droga
Endotélio Vascular/metabolismo
Feminino
Seres Humanos
Masculino
Meia-Idade
Coelhos
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzimidazoles); 0 (Benzoates); 11128-99-7 (Angiotensin II); U5SYW473RQ (telmisartan)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180110
[St] Status:MEDLINE
[do] DOI:10.1002/cbf.3313


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[PMID]:29339068
[Au] Autor:Lu Y; Wu F
[Ad] Endereço:Department of Pediatrics, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China.
[Ti] Título:A new miRNA regulator, miR-672, reduces cardiac hypertrophy by inhibiting JUN expression.
[So] Source:Gene;648:21-30, 2018 Mar 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Cardiac hypertrophy is one of the initial symptoms of many heart diseases. We found that miR-672-5p may participate in the regulation of heart disease development in mouse, but the association between miR-672-5p and cardiac hypertrophy remains unclear. In the present study, we found that the abundance of miR-672-5p decreased in hypertrophic cardiomyocytes induced by phenylephrine, angiotensin II (Ang II) and insulin-like growth factor 1. Putative target genes of miR-672-5p were identified using four pipelines, miRWalk, miRanda, RNA22 and Targetscan, and a total of 834 genes were predicted by all four pipelines. Among these target genes, 98 were associated with the development of heart disease. PPI networks showed that the Jun proto-oncogene product (JUN), a subunit of the AP-1 transcription factor, had the highest node degree, and it was defined as the hub gene of the PPI networks. Luciferase assays showed that miR-672-5p bound to the 3' UTR of the JUN gene and decreased luciferase activity, indicating that JUN is a target of miR-672-5p. Finally, we found that increasing the abundance of miR-672-5p in cardiomyocytes controlled the relative cell area in Ang II-stimulated hypertrophic cardiomyocytes. Correspondingly, the abundance of JUN, a target of miR-672-5p, was decreased in hypertrophic cardiomyocytes on both mRNA and protein levels, implying that miR-672-5p had suppressive effects on cardiac hypertrophy through regulating the expression of Jun in cardiomyocytes.
[Mh] Termos MeSH primário: Cardiomegalia/genética
Regulação da Expressão Gênica
MicroRNAs/genética
Proteínas Proto-Oncogênicas c-jun/genética
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/genética
Angiotensina II/farmacologia
Animais
Animais Recém-Nascidos
Cardiomegalia/metabolismo
Células Cultivadas
Perfilação da Expressão Gênica/métodos
Ontologia Genética
Camundongos Endogâmicos ICR
MicroRNAs/metabolismo
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Proteínas Proto-Oncogênicas c-jun/metabolismo
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (MIRN672 microRNA, rat); 0 (MicroRNAs); 0 (Proto-Oncogene Proteins c-jun); 11128-99-7 (Angiotensin II)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180226
[Lr] Data última revisão:
180226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE


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[PMID]:29202139
[Au] Autor:Nowinska P; Kasacka I
[Ad] Endereço:Department of Histology and Cytophysiology, Medical University of Bialystok, Bialystok, Poland.
[Ti] Título:Changes in the pancreas caused by different types of hypertension.
[So] Source:Acta Biochim Pol;64(4):591-595, 2017.
[Is] ISSN:1734-154X
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Hypertension is considered a lifestyle disease. Unfavorable forecasts predict a significant increase in the number of patients suffering from this disorder. Many changes in various organs have been observed as a result of ischemia. An interesting question arises of whether differences between the mechanisms occurring in different types of hypertension could produce different effects in the organs. It is well known that there is a close relationship between hypertension and insulin resistance. On the other hand, insulin resistance is the main cause of type 2 diabetes, which develops in parallel with changes in the pancreas. The pancreas is a very important organ since it produces enzymes crucial for the digestive process, as well as performs an important endocrine function. The work presented here focuses primarily on the latter issue. The authors present an overview of contemporary literature concerning the influence of different types of hypertension on the function of the pancreas.
[Mh] Termos MeSH primário: Hipertensão/fisiopatologia
Pâncreas/fisiopatologia
[Mh] Termos MeSH secundário: Angiotensina II/metabolismo
Diabetes Mellitus Tipo 2/etiologia
Seres Humanos
Hipertensão/complicações
Hipertensão/etiologia
Resistência à Insulina
Pâncreas/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
11128-99-7 (Angiotensin II)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.18388/abp.2017_1504


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[PMID]:29185789
[Au] Autor:Mou Y; Zhang Y; Guo C; Zhao J; Zhang Z; Zhou X; Dong J; Liao L
[Ad] Endereço:1 Division of Cardiology, Department of Internal Medicine, Shandong Provincial Hospital Affiliated to Shandong University , Jinan, China .
[Ti] Título:Integrated Treatment of Prostaglandin E1 and Angiotensin-Converting Enzyme Inhibitor in Diabetic Kidney Disease Rats: Possible Role of Antiapoptosis in Renal Tubular Epithelial Cells.
[So] Source:DNA Cell Biol;37(2):133-141, 2018 Feb.
[Is] ISSN:1557-7430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:To investigate the therapeutic mechanisms underlying prostaglandin E1 (PGE1) and angiotensin-converting enzyme inhibitor (ACEI) on reducing urinary protein in diabetic kidney disease (DKD). DKD rats were established and randomly divided into four groups: PGE1 (10 µg/kg/day) (P group), ACEI (10 mg/kg/day) (A group), combination of PGE1 with ACEI treatment (P + A group), and saline treatment group (DKD group). Untreated rats were used as normal control (N group). Urinary albumin, endothelin-1 (ET-1), angiotensin II (AngII), TUNEL assay, Masson's trichrome staining, and immunohistochemistry staining for CD68 were evaluated in all groups. Ten days after treatment, urinary albumin was significantly decreased in the P and P + A groups (p < 0.01 vs. the DKD group). At the end of 8 weeks, the albumin was still significantly reduced in the P + A group (p < 0.05 vs. the A group). ET-1 and AngII were also significantly decreased in three treatment groups (p < 0.01 vs. the DKD group), especially in the P + A group. Few cells underwent apoptosis in glomerular regions in DKD rats, while amounts of apoptotic cells were seen in tubules regions. Further, apoptosis and the areas of fibrosis in tubulointerstitial were both decreased most in the P + A group compared with the DKD group. Apoptosis of renal tubular epithelial cells may participate in the development and progression of DKD in rats. Combination of PGE1 with AGEI remarkably protects renal function compared with PGE1 or ACEI monotherapy. The potential therapeutic mechanisms of PGE1 and AGEI might be via multiple targets and, at least in part, through inhibiting the apoptosis of renal tubular epithelial cells.
[Mh] Termos MeSH primário: Alprostadil/farmacologia
Inibidores da Enzima Conversora de Angiotensina/farmacologia
Diabetes Mellitus Experimental/complicações
Nefropatias Diabéticas/tratamento farmacológico
Nefrite Intersticial/tratamento farmacológico
[Mh] Termos MeSH secundário: Angiotensina II/sangue
Animais
Apoptose/efeitos dos fármacos
Diabetes Mellitus Experimental/sangue
Nefropatias Diabéticas/sangue
Nefropatias Diabéticas/etiologia
Avaliação Pré-Clínica de Medicamentos
Endotelina-1/sangue
Células Epiteliais/efeitos dos fármacos
Túbulos Renais/efeitos dos fármacos
Túbulos Renais/patologia
Macrófagos/imunologia
Masculino
Nefrite Intersticial/sangue
Nefrite Intersticial/etiologia
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiotensin-Converting Enzyme Inhibitors); 0 (Endothelin-1); 11128-99-7 (Angiotensin II); F5TD010360 (Alprostadil)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE
[do] DOI:10.1089/dna.2017.3690


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[PMID]:29346401
[Au] Autor:van Puijvelde GHM; Foks AC; van Bochove RE; Bot I; Habets KLL; de Jager SC; Ter Borg MND; van Osch P; Boon L; Vos M; de Waard V; Kuiper J
[Ad] Endereço:Division of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands.
[Ti] Título:CD1d deficiency inhibits the development of abdominal aortic aneurysms in LDL receptor deficient mice.
[So] Source:PLoS One;13(1):e0190962, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:An abdominal aortic aneurysm (AAA) is a dilatation of the abdominal aorta leading to serious complications and mostly to death. AAA development is associated with an accumulation of inflammatory cells in the aorta including NKT cells. An important factor in promoting the recruitment of these inflammatory cells into tissues and thereby contributing to the development of AAA is angiotensin II (Ang II). We demonstrate that a deficiency in CD1d dependent NKT cells under hyperlipidemic conditions (LDLr-/-CD1d-/- mice) results in a strong decline in the severity of angiotensin II induced aneurysm formation when compared with LDLr-/- mice. In addition, we show that Ang II amplifies the activation of NKT cells both in vivo and in vitro. We also provide evidence that type I NKT cells contribute to AAA development by inducing the expression of matrix degrading enzymes in vSMCs and macrophages, and by cytokine dependently decreasing vSMC viability. Altogether, these data prove that CD1d-dependent NKT cells contribute to AAA development in the Ang II-mediated aneurysm model by enhancing aortic degradation, establishing that therapeutic applications which target NKT cells can be a successful way to prevent AAA development.
[Mh] Termos MeSH primário: Antígenos CD1d/genética
Aneurisma da Aorta Abdominal/prevenção & controle
Receptores de LDL/genética
[Mh] Termos MeSH secundário: Angiotensina II/administração & dosagem
Animais
Apoptose/imunologia
Citometria de Fluxo
Ativação Linfocitária
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Músculo Liso Vascular/imunologia
Músculo Liso Vascular/patologia
Células NIH 3T3
Células T Matadoras Naturais/imunologia
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Antigens, CD1d); 0 (Cd1d1 protein, mouse); 0 (Receptors, LDL); 11128-99-7 (Angiotensin II)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180221
[Lr] Data última revisão:
180221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180119
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0190962


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[PMID]:29203630
[Au] Autor:Touyz RM; Montezano AC
[Ad] Endereço:From the Institute of Cardiovascular and Medical Sciences, University of Glasgow, United Kingdom. rhian.touyz@glasgow.ac.uk.
[Ti] Título:Angiotensin-(1-7) and Vascular Function: The Clinical Context.
[So] Source:Hypertension;71(1):68-69, 2018 01.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Angiotensina I
Fragmentos de Peptídeos
[Mh] Termos MeSH secundário: Angiotensina II
Seres Humanos
Músculo Liso Vascular
[Pt] Tipo de publicação:EDITORIAL; RESEARCH SUPPORT, NON-U.S. GOV'T; COMMENT
[Nm] Nome de substância:
0 (Peptide Fragments); 11128-99-7 (Angiotensin II); 9041-90-1 (Angiotensin I); IJ3FUK8MOF (angiotensin I (1-7))
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.10406


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[PMID]:29296021
[Au] Autor:Li T; Yu B; Liu Z; Li J; Ma M; Wang Y; Zhu M; Yin H; Wang X; Fu Y; Yu F; Wang X; Fang X; Sun J; Kong W
[Ad] Endereço:Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing, 100191, China.
[Ti] Título:Homocysteine directly interacts and activates the angiotensin II type I receptor to aggravate vascular injury.
[So] Source:Nat Commun;9(1):11, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hyperhomocysteinemia (HHcy) is a risk factor for various cardiovascular diseases. However, the mechanism underlying HHcy-aggravated vascular injury remains unclear. Here we show that the aggravation of abdominal aortic aneurysm by HHcy is abolished in mice with genetic deletion of the angiotensin II type 1 (AT1) receptor and in mice treated with an AT1 blocker. We find that homocysteine directly activates AT1 receptor signalling. Homocysteine displaces angiotensin II and limits its binding to AT1 receptor. Bioluminescence resonance energy transfer analysis reveals distinct conformational changes of AT1 receptor upon binding to angiotensin II and homocysteine. Molecular dynamics and site-directed mutagenesis experiments suggest that homocysteine regulates the conformation of the AT1 receptor both orthosterically and allosterically by forming a salt bridge and a disulfide bond with its Arg and Cys residues, respectively. Together, these findings suggest that strategies aimed at blocking the AT1 receptor may mitigate HHcy-associated aneurysmal vascular injuries.
[Mh] Termos MeSH primário: Aneurisma da Aorta Abdominal/metabolismo
Homocisteína/metabolismo
Receptor Tipo 1 de Angiotensina/metabolismo
[Mh] Termos MeSH secundário: Regulação Alostérica
Angiotensina I/metabolismo
Angiotensina II/metabolismo
Animais
Células HEK293
Seres Humanos
Masculino
Camundongos Endogâmicos C57BL
Simulação de Dinâmica Molecular
Mutagênese Sítio-Dirigida
Conformação Proteica
Lesões do Sistema Vascular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptor, Angiotensin, Type 1); 0LVT1QZ0BA (Homocysteine); 11128-99-7 (Angiotensin II); 9041-90-1 (Angiotensin I)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02401-7


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[PMID]:29225168
[Au] Autor:Chai H; Tao Z; Chen W; Xu Y; Huang F; Su C; Chen X
[Ad] Endereço:The Department of Thoracic and Cardiovascular Surgery, Nanjing First Hospital, Nanjing Medical University, Changle Road 68, Nanjing 210006, Jiangsu, People's Republic of China.
[Ti] Título:Cortistatin attenuates angiotensin II-induced abdominal aortic aneurysm through inactivation of the ERK1/2 signaling pathways.
[So] Source:Biochem Biophys Res Commun;495(2):1801-1806, 2018 01 08.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Abdominal aortic aneurysm (AAA) is a fatal disease that is associated with chronic inflammation in the vessel wall. Cortistatin is implicated in inflammation, vascular smooth muscle cell migration and other cardiovascular pathologies. But, the hypothetical effect of cortistatin on AAA remains uncertain. We investigated the effect of cortistatin administration to angiotensin (Ang) II-induced AAA formation in apolipoprotein E deficient (Apoe ) mice. We showed that cortistatin administration significantly suppresses incidence and severity of AAA in Apoe mice. A significant increase in macrophage infiltration, excretion of inflammatory cytokines, activities and expression levels of MMP2 and MMP9, reactive oxygen species levels and cell apoptosis in aneurysmal aortic wall of Apoe mice infused with Ang-II, and these events were significantly alleviated by co-treatment with cortistatin. Mechanistic studies showed that the protective effects of cortistatin were related to the blocking of ERK1/2 signaling pathways, while does not was not actually affect JNK, P38 phosphorylation. In conclusion, cortistatin appears to play an essential role in the formation of AAA and indicate cortistatin may as novel therapeutic option for AAA.
[Mh] Termos MeSH primário: Aneurisma da Aorta Abdominal/prevenção & controle
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Neuropeptídeos/administração & dosagem
[Mh] Termos MeSH secundário: Angiotensina II/administração & dosagem
Animais
Aorta Abdominal/efeitos dos fármacos
Aorta Abdominal/metabolismo
Aorta Abdominal/patologia
Aneurisma da Aorta Abdominal/etiologia
Aneurisma da Aorta Abdominal/metabolismo
Apoptose/efeitos dos fármacos
Linhagem Celular
Modelos Animais de Doenças
Elastina/metabolismo
Masculino
Metaloproteinase 2 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Camundongos
Camundongos Knockout para ApoE
Miócitos de Músculo Liso/efeitos dos fármacos
Miócitos de Músculo Liso/patologia
Proteólise/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuropeptides); 0 (Reactive Oxygen Species); 0 (cortistatin); 11128-99-7 (Angiotensin II); 9007-58-3 (Elastin); EC 3.4.24.24 (Matrix Metalloproteinase 2); EC 3.4.24.24 (Mmp2 protein, mouse); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE


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[PMID]:28461606
[Au] Autor:Ueki N; Kanasaki K; Kanasaki M; Takeda S; Koya D
[Ad] Endereço:From the Department of Obstetrics and Gynecology, Juntendo University, Tokyo, Japan (N.U., S.T.); and Department of Diabetology and Endocrinology (N.U., K.K., M.K., D.K.) and Division of Anticipatory Molecular Food Science and Technology, Medical Research Institute (K.K., D.K.), Kanazawa Medical Uni
[Ti] Título:Catechol-O-Methyltransferase Deficiency Leads to Hypersensitivity of the Pressor Response Against Angiotensin II.
[So] Source:Hypertension;69(6):1156-1164, 2017 06.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Catechol-O-methyltransferase (COMT) metabolizes 2-hydroxyestradiol into 2-methoxyestradiol (2-ME); COMT deficiency has shown to be associated with hypertension in men and preeclampsia, the disease associated with hypersensitivity of pressor response against angiotensin II (Ang II). Here, we found that COMT deficiency could explain the hypersensitivity of pressor response against Ang II in mice because of the lack of 2-ME-dependent suppression of angiotensin II receptor type 1 (AT1R). Male C57BL/6 mice were subjected to COMT inhibitor (COMTi: 25 mg/kg per day) or oil (control) for 4 weeks, with or without low-dose Ang II infusion (ANGII: 70 ng/kg per minute) for the last 3 weeks. The Ang II-infused mice were treated with 2-ME (10 ng/d) or vehicle for the last 1 week. We obtained the following experimental groups: control, ANGII, COMTi, COMTi+ANGII, and COMTi+ANGII+2-ME. We performed similar experiments using the in vivo administration of small interfering RNA of COMT instead of COMTi. Neither ANGII nor COMTi exhibited significant alterations in systolic blood pressure. Compared with ANGII or COMTi, COMTi+ANGII displayed significantly higher systolic blood pressure, albuminuria, and glomerular endotheliosis; 2-ME normalized such alterations. Similar phenotypes were observed in COMT small interfering RNA-treated mice. In the aorta of COMT-deficient mice, AT1R expression was increased; 2-ME suppressed AT1R expression. The 2-ME exhibited peroxisome proliferator-activated receptor γ agonistic activity in vitro and ex vivo plasma from pregnant female mice as well. In vitro, 2-ME suppressed both basal and Ang II-induced AT1R levels in a peroxisome proliferator-activated receptor γ-dependent manner. The 2-ME is relevant to combat COMT deficiency-associated hypertensive disorders via suppression of AT1R by its peroxisome proliferator-activated receptor γ activity.
[Mh] Termos MeSH primário: Angiotensina II/farmacologia
Catecol O-Metiltransferase/deficiência
Hipersensibilidade a Drogas/fisiopatologia
Pré-Eclâmpsia/fisiopatologia
Prenhez
Tiazolidinedionas/farmacologia
[Mh] Termos MeSH secundário: Animais
Feminino
Hipertensão/tratamento farmacológico
Hipertensão/fisiopatologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
PPAR gama/metabolismo
Pré-Eclâmpsia/tratamento farmacológico
Gravidez
Receptor Tipo 1 de Angiotensina/metabolismo
Valores de Referência
Vasoconstritores/farmacologia
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (PPAR gamma); 0 (Receptor, Angiotensin, Type 1); 0 (Thiazolidinediones); 0 (Vasoconstrictor Agents); 11128-99-7 (Angiotensin II); EC 2.1.1.6 (Catechol O-Methyltransferase); X4OV71U42S (pioglitazone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180113
[Lr] Data última revisão:
180113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09247


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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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