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[PMID]:29237697
[Au] Autor:Roucher-Boulez F; Brac de la Perriere A; Jacquez A; Chau D; Guignat L; Vial C; Morel Y; Nicolino M; Raverot G; Pugeat M
[Ad] Endereço:Laboratoire de Biochimie et Biologie Moléculaire Grand EstUM Pathologies Endocriniennes Rénales Musculaires et Mucoviscidose, Groupement Hospitalier Est, Hospices Civils de Lyon, Bron, France florence.roucher@chu-lyon.fr.
[Ti] Título:Triple-A syndrome: a wide spectrum of adrenal dysfunction.
[So] Source:Eur J Endocrinol;178(3):199-207, 2018 Mar.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Triple-A or Allgrove syndrome is an autosomal recessive disorder due to mutations in the gene, which encodes a nucleoporin named ALADIN. It is characterized by a classical clinical triad: alacrima, achalasia and adrenal insufficiency, the canonic symptoms that are associated with progressive peripheral neuropathy. Only a few cohorts have been reported. The objective of the present study was to characterize the various spectra of adrenal function in Triple-A patients. METHODS: A retrospective clinical and biological monitoring of 14 patients (10 families) was done in a single multidisciplinary French center. All had gene sequenced and adrenal function evaluation. RESULTS: Nine different mutations were found, including one new mutation: c.755G>C, p.(Trp252Ser). Regarding adrenal function, defects of the zona fasciculata and reticularis were demonstrated by increased basal ACTH levels and low DHEAS levels in all cases regardless of the degree of glucocorticoid deficiency. In contrast, mineralocorticoid function was always conserved: i.e., normal plasma renin level associated with normal aldosterone level. The main prognostic feature was exacerbation of neuropathy and cognitive disorders. CONCLUSIONS: These data suggest that, in Triple-A patients, adrenal function can be deficient, insufficient or compensated. In our cohort after the first decade of life, there does not appear to be any degradation of adrenal function over time. However, patients with compensated adrenal function should be informed and educated to manage a glucocorticoid replacement therapy in case of stressful conditions, with no need for systematic long-term treatment.
[Mh] Termos MeSH primário: Insuficiência Adrenal/genética
Acalasia Esofágica/genética
Proteínas do Tecido Nervoso/genética
Complexo de Proteínas Formadoras de Poros Nucleares/genética
[Mh] Termos MeSH secundário: Adolescente
Insuficiência Adrenal/complicações
Insuficiência Adrenal/metabolismo
Insuficiência Adrenal/fisiopatologia
Hormônio Adrenocorticotrópico/metabolismo
Adulto
Idoso
Aldosterona/metabolismo
Criança
Transtornos Cognitivos/etiologia
Transtornos Cognitivos/fisiopatologia
Transtornos Cognitivos/psicologia
Estudos de Coortes
Sulfato de Desidroepiandrosterona/metabolismo
Progressão da Doença
Acalasia Esofágica/complicações
Acalasia Esofágica/metabolismo
Acalasia Esofágica/fisiopatologia
Feminino
França
Glucocorticoides/deficiência
Seres Humanos
Masculino
Meia-Idade
Doenças do Sistema Nervoso Periférico/etiologia
Doenças do Sistema Nervoso Periférico/fisiopatologia
Fenótipo
Prognóstico
Renina/metabolismo
Estudos Retrospectivos
Adulto Jovem
Zona Fasciculada/metabolismo
Zona Reticular/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AAAS protein, human); 0 (Glucocorticoids); 0 (Nerve Tissue Proteins); 0 (Nuclear Pore Complex Proteins); 4964P6T9RB (Aldosterone); 57B09Q7FJR (Dehydroepiandrosterone Sulfate); 9002-60-2 (Adrenocorticotropic Hormone); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0642


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[PMID]:29232382
[Au] Autor:McClelland AD; Lichtnekert J; Eng DG; Pippin JW; Gross KW; Gharib SA; Shankland SJ
[Ad] Endereço:Division of Nephrology, University of Washington, Seattle, Washington, United States of America.
[Ti] Título:Charting the transcriptional landscape of cells of renin lineage following podocyte depletion.
[So] Source:PLoS One;12(12):e0189084, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Renin producing cells of the juxtaglomerulus, herein called cells of renin lineage (CoRL), have garnered recent interest for their propensity to act as a progenitor source for various kidney cell types including podocytes. Despite recent advances, the process of transdifferentiation of CoRL to podocytes is poorly understood. In this study, we employed a transgenic reporter mouse line which permanently labels CoRL with ZsGreen fluorescent protein, allowing for isolation by fluorescence-activated cell sorting. At 5 days following induction of abrupt podocyte ablation via anti-podocyte sheep IgG, mice were sacrificed and CoRL were isolated by FACS. RNA was subsequently analyzed by microarray. Gene set enrichment analysis (GSEA) was performed and revealed that CoRL display a distinct phenotype following podocyte ablation, primarily consisting of downregulation of metabolic processes and upregulation of immuno-modulatory processes. Additionally, RNA-biology and cell cycle-related processes were also upregulated. Changes in gene expression or activity of a core set of transcription factors including HNF1 and E2F were identified through changes in enrichment of their respective target genes. However, integration of results from transcription factor and canonical pathway analysis indicated that ERR1 and PU-box family members may be the major contributors to the post-podocyte ablation phenotype of CoRL. Finally, top ranking genes were selected from the microarray-based analysis and confirmed by qPCR. Collectively, our results provide valuable insights into the transcriptional regulation of CoRL following abrupt podocyte ablation.
[Mh] Termos MeSH primário: Linhagem da Célula
Podócitos/metabolismo
Renina/biossíntese
Transcrição Genética
[Mh] Termos MeSH secundário: Animais
Separação Celular
Citometria de Fluxo
Regulação da Expressão Gênica
Córtex Renal/citologia
Córtex Renal/metabolismo
Camundongos
Camundongos Transgênicos
Podócitos/citologia
RNA/isolamento & purificação
Reação em Cadeia da Polimerase em Tempo Real
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Transcription Factors); 63231-63-0 (RNA); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189084


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[PMID]:29240788
[Au] Autor:Tripathi R; Sullivan R; Fan TM; Wang D; Sun Y; Reed GL; Gladysheva IP
[Ad] Endereço:Departments of Medicine, University of Tennessee Health Science Center, Memphis, Tennessee, United States of America.
[Ti] Título:Enhanced heart failure, mortality and renin activation in female mice with experimental dilated cardiomyopathy.
[So] Source:PLoS One;12(12):e0189315, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Dilated cardiomyopathy (DCM) is the major cause of heart failure affecting both women and men. Limited clinical studies show conflicting data in sex-related differences in the progression of dilated cardiomyopathy and heart failure (HF) outcomes. We examined the comparative sex-related progression of cardiomyopathy and the development of HF (at 4, 7, 13 weeks of age) in a well-established, transgenic mouse model of DCM that recapitulates the progressive stages of human HF. By 13 weeks of age, female mice with DCM had more severe left ventricular systolic dysfunction, left ventricular dilation and wall thinning (P<0.001 for all) than age-matched male mice with DCM. Female mice also had greater lung edema (P<0.001), cardiac fibrosis (P<0.01) and pleural effusions, which were not rescued by ovariectomy. By comparison to DCM male mice at 13 weeks, these pathological changes in female mice with DCM, were associated with significant increases in plasma active renin (P<0.01), angiotensin II (P<0.01) and aldosterone levels (P<0.001). In comparison to DCM male mice, DCM female mice also showed differential expression of the natriuretic peptide system with lower corin and higher ANP, BNP and cGMP levels at 13 weeks of age. We conclude, that female mice with experimental DCM have an accelerated progression of cardiomyopathy and HF, which was not corrected by early ovariectomy. These alterations are associated with early renin activation with increased angiotensin II and aldosterone levels, and altered expression of the natriuretic peptide system.
[Mh] Termos MeSH primário: Cardiomiopatia Dilatada/fisiopatologia
Insuficiência Cardíaca/fisiopatologia
Renina/metabolismo
[Mh] Termos MeSH secundário: Animais
Cardiomiopatia Dilatada/metabolismo
Cardiomiopatia Dilatada/mortalidade
Feminino
Insuficiência Cardíaca/metabolismo
Insuficiência Cardíaca/mortalidade
Masculino
Camundongos
Camundongos Transgênicos
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189315


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[PMID]:29052707
[Au] Autor:Brown JM; Robinson-Cohen C; Luque-Fernandez MA; Allison MA; Baudrand R; Ix JH; Kestenbaum B; de Boer IH; Vaidya A
[Ad] Endereço:From Brigham and Women's Hospital and Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Vanderbilt University, Nashville, Tennessee; University of Washington, Seattle, Washington; London School of Hygiene & Tropical Medicine, London, United Kingdom; Pontificia Universidad Católic
[Ti] Título:The Spectrum of Subclinical Primary Aldosteronism and Incident Hypertension: A Cohort Study.
[So] Source:Ann Intern Med;167(9):630-641, 2017 Nov 07.
[Is] ISSN:1539-3704
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Background: Primary aldosteronism is recognized as a severe form of renin-independent aldosteronism that results in excessive mineralocorticoid receptor (MR) activation. Objective: To investigate whether a spectrum of subclinical renin-independent aldosteronism that increases risk for hypertension exists among normotensive persons. Design: Cohort study. Setting: National community-based study. Participants: 850 untreated normotensive participants in MESA (Multi-Ethnic Study of Atherosclerosis) with measurements of serum aldosterone and plasma renin activity (PRA). Measurements: Longitudinal analyses investigated whether aldosterone concentrations, in the context of physiologic PRA phenotypes (suppressed, ≤0.50 µg/L per hour; indeterminate, 0.51 to 0.99 µg/L per hour; unsuppressed, ≥1.0 µg/L per hour), were associated with incident hypertension (defined as systolic blood pressure ≥140 mm Hg, diastolic blood pressure ≥90 mm Hg, or initiation of antihypertensive medications). Cross-sectional analyses investigated associations between aldosterone and MR activity, assessed via serum potassium and urinary fractional excretion of potassium. Results: A suppressed renin phenotype was associated with a higher rate of incident hypertension than other PRA phenotypes (incidence rates per 1000 person-years of follow-up: suppressed renin phenotype, 85.4 events [95% CI, 73.4 to 99.3 events]; indeterminate renin phenotype, 53.3 events [CI, 42.8 to 66.4 events]; unsuppressed renin phenotype, 54.5 events [CI, 41.8 to 71.0 events]). With renin suppression, higher aldosterone concentrations were independently associated with an increased risk for incident hypertension, whereas no association between aldosterone and hypertension was seen when renin was not suppressed. Higher aldosterone concentrations were associated with lower serum potassium and higher urinary excretion of potassium, but only when renin was suppressed. Limitation: Sodium and potassium were measured several years before renin and aldosterone. Conclusion: Suppression of renin and higher aldosterone concentrations in the context of this renin suppression are associated with an increased risk for hypertension and possibly also with increased MR activity. These findings suggest a clinically relevant spectrum of subclinical primary aldosteronism (renin-independent aldosteronism) in normotension. Primary Funding Source: National Institutes of Health.
[Mh] Termos MeSH primário: Hiperaldosteronismo/complicações
Hipertensão/complicações
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Aldosterona/sangue
Estudos Transversais
Feminino
Seres Humanos
Hiperaldosteronismo/sangue
Hipertensão/epidemiologia
Incidência
Estudos Longitudinais
Masculino
Meia-Idade
Potássio/sangue
Potássio/urina
Receptores de Mineralocorticoides/metabolismo
Renina/sangue
Fatores de Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Receptors, Mineralocorticoid); 4964P6T9RB (Aldosterone); EC 3.4.23.15 (Renin); RWP5GA015D (Potassium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE
[do] DOI:10.7326/M17-0882


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[PMID]:29050562
[Au] Autor:Polhemus DJ; Trivedi RK; Gao J; Li Z; Scarborough AL; Goodchild TT; Varner KJ; Xia H; Smart FW; Kapusta DR; Lefer DJ
[Ad] Endereço:Cardiovascular Center of Excellence, Louisiana State University (LSU) Health Sciences Center, New Orleans, Louisiana; Department of Pharmacology and Experimental Therapeutics, LSU Health Sciences Center, New Orleans, Louisiana.
[Ti] Título:Renal Sympathetic Denervation Protects the Failing Heart Via Inhibition of Neprilysin Activity in the Kidney.
[So] Source:J Am Coll Cardiol;70(17):2139-2153, 2017 Oct 24.
[Is] ISSN:1558-3597
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sustained sympathetic activation contributes to the progression of myocardial cell injury, cardiac fibrosis, and left ventricular (LV) dysfunction in heart failure (HF). OBJECTIVES: This study investigated the effects of radiofrequency renal nerve denervation (RF-RDN) on the pathobiology of HF and the interaction between the renal sympathetic nerves and natriuretic peptide (NP) metabolism. METHODS: Spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) were subjected to 45 min of coronary artery ligation and reperfusion for 12 weeks. At 4 weeks post-reperfusion, SHR and WKY underwent either bilateral RF-RDN or sham-RDN. RESULTS: Following RF-RDN in both strains, LV ejection fraction remained significantly above those levels in respective sham-RDN rats, and at the end of the 12-week study, rats in both strains had significantly reduced LV fibrosis and improved vascular function. RF-RDN therapy significantly improved vascular reactivity to endothelium-dependent and -independent vasodilators as well as vascular compliance in the setting of severe HF. Improvements in LV function were accompanied by significant elevations in circulating NP as compared to those associated with sham-RDN. Further investigation into the cause of increased circulating NP levels demonstrated that RF-RDN significantly inhibited renal neprilysin activity in SHR and WKY with HF. Likewise, chronic treatment with the beta antagonist bisoprolol inhibited renal neprilysin activity and increased circulation NP levels in WKY with HF. CONCLUSIONS: This study identifies a novel endogenous pathway by which the renal nerves participate in the degradation of cardioprotective NP. Furthermore, removal of the influence of the renal nerves on kidney function attenuates renal neprilysin activity, augments circulating NP levels, reduces myocardial fibrosis, and improves LV function in the setting of HF.
[Mh] Termos MeSH primário: Insuficiência Cardíaca/terapia
Rim/inervação
Neprilisina/antagonistas & inibidores
Simpatectomia
[Mh] Termos MeSH secundário: Aminobutiratos/farmacologia
Angiotensina II/sangue
Animais
Bisoprolol/farmacologia
Pressão Sanguínea
Ecocardiografia
Miocárdio/química
Miocárdio/patologia
Neprilisina/fisiologia
Nitritos/análise
Norepinefrina/sangue
Ratos
Ratos Endogâmicos SHR
Ratos Endogâmicos WKY
Artéria Renal/inervação
Renina/sangue
Traumatismo por Reperfusão/fisiopatologia
Tetrazóis/farmacologia
Função Ventricular Esquerda/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (LCZ 696); 0 (Nitrites); 0 (Tetrazoles); 11128-99-7 (Angiotensin II); EC 3.4.23.15 (Renin); EC 3.4.24.11 (Neprilysin); X4W3ENH1CV (Norepinephrine); Y41JS2NL6U (Bisoprolol)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE


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[PMID]:28918839
[Au] Autor:Salinas-Parra N; Reyes-Martínez C; Prieto MC; Gonzalez AA
[Ad] Endereço:Instituto de Química, Pontificia Universidad Católica de Valparaíso, Valparaíso, Chile.
[Ti] Título:Prostaglandin E Induces Prorenin-Dependent Activation of (Pro)renin Receptor and Upregulation of Cyclooxygenase-2 in Collecting Duct Cells.
[So] Source:Am J Med Sci;354(3):310-318, 2017 Sep.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Prostaglandin E2 (PGE ) regulates renin expression in renal juxtaglomerular cells. PGE acts through E-prostanoid (EP) receptors in the renal collecting duct (CD) to regulate sodium and water balance. CD cells express EP1 and EP4, which are linked to protein kinase C (PKC) and PKA downstream pathways, respectively. Previous studies showed that the presence of renin in the CD, and that of PKC and PKA pathways, activate its expression. The (pro)renin receptor (PRR) is also expressed in CD cells, and its activation enhances cyclooxygenase-2 (COX-2) through extracellular signal-regulated kinase (ERK). We hypothesized that PGE stimulates prorenin and renin synthesis leading to subsequent activation of PRR and upregulation of COX-2. METHODS: We used a mouse M-1 CD cell line that expresses EP1, EP3 and EP4 but not EP2. RESULTS: PGE (10 M) treatment increased prorenin and renin protein levels at 4 and 8 hours. No differences were found at 12-hour after PGE treatment. Phospho-ERK was significantly augmented after 12 hours. COX-2 expression was decreased after 4 hours of PGE treatment, but increased after 12 hours. Interestingly, the full-length form of the PRR was upregulated only at 12 hours. PGE -mediated phospho-ERK and COX-2 upregulation was suppressed by PRR silencing. CONCLUSIONS: Our results suggest that PGE induces biphasic regulation of COX-2 through renin-dependent PRR activation via EP1 and EP4 receptors. PRR-mediated increases in COX-2 expression may enhance PGE synthesis in CD cells serving as a buffer mechanism in conditions of activated renin-angiotensin system.
[Mh] Termos MeSH primário: Ciclo-Oxigenase 2/biossíntese
Dinoprostona/farmacologia
Túbulos Renais Coletores/efeitos dos fármacos
Receptores de Superfície Celular/metabolismo
Renina/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Técnicas de Cultura de Células
Linhagem Celular
Técnicas de Silenciamento de Genes
Túbulos Renais Coletores/citologia
Túbulos Renais Coletores/metabolismo
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Camundongos
Fosforilação
Receptores de Superfície Celular/genética
Receptores de Prostaglandina E/biossíntese
Fatores de Tempo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Cell Surface); 0 (Receptors, Prostaglandin E); 0 (prorenin receptor); EC 1.14.99.- (Ptgs2 protein, mouse); EC 1.14.99.1 (Cyclooxygenase 2); EC 3.4.23.15 (Renin); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171028
[Lr] Data última revisão:
171028
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE


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[PMID]:28893641
[Au] Autor:de Oliveira Sá G; Dos Santos Neves V; de Oliveira Fraga SR; Souza-Mello V; Barbosa-da-Silva S
[Ad] Endereço:Institute of Biology, State University of Rio de Janeiro, RJ, Brazil.
[Ti] Título:High-intensity interval training has beneficial effects on cardiac remodeling through local renin-angiotensin system modulation in mice fed high-fat or high-fructose diets.
[So] Source:Life Sci;189:8-17, 2017 Nov 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: HIIT (high-intensity interval training) has the potential to reduce cardiometabolic risk factors, but the effects on cardiac remodeling and local RAS (renin-angiotensin system) in mice fed high-fat or high-fructose diets still need to be fully addressed. MAIN METHODS: Sixty male C57BL/6 mice (12weeks old) were randomly divided into three groups, control (C), High-fat (HF), or High-fructose diet (HRU) and were monitored for eight weeks before being submitted to the HIIT. Each group was randomly assigned to 2 subgroups, one subgroup was started on a 12-week HIIT protocol (T=trained group), while the other subgroup remained non-exercised (NT=not-trained group). KEY FINDINGS: HIIT reduced BM and systolic blood pressure in high-fat groups, while enhanced insulin sensitivity after high-fat or high-fructose intake. Moreover, HIIT reduced left ventricular hypertrophy in HF-T and HFRU-T. Notably, HIIT modulated key factors in the local left ventricular renin-angiotensin-system (RAS): reduced protein expression of renin, ACE (Angiotensin-converting enzyme), and (Angiotensin type 2 receptor) AT2R in HF-T and HFRU-T groups but reduced (Angiotensin type 1 receptor) AT1R protein expression only in the high-fat trained group. HIIT modulated ACE2/Ang (1-7)/Mas receptor axis. ACE2 mRNA gene expression was enhanced in HF-T and HFRU-T groups, complying with elevated Mas (Mas proto-oncogene, G protein-coupled receptor) receptor mRNA gene expression after HIIT. SIGNIFICANCE: This study shows the effectiveness of HIIT sessions in producing improvements in insulin sensitivity and mitigating LV hypertrophy, though hypertension was controlled only in the high-fat-fed submitted to HIIT protocol. Local RAS system in the heart mediates these findings and receptor MAS seems to play a pivotal role when it comes to the amelioration of cardiac structural and functional remodeling due to HIIT.
[Mh] Termos MeSH primário: Treinamento Intervalado de Alta Intensidade
Hipertrofia Ventricular Esquerda/terapia
Resistência à Insulina/fisiologia
Sistema Renina-Angiotensina/fisiologia
Remodelação Ventricular/fisiologia
[Mh] Termos MeSH secundário: Angiotensina I/metabolismo
Animais
Pressão Sanguínea/fisiologia
Dieta Hiperlipídica
Frutose
Regulação da Expressão Gênica/fisiologia
Hipertensão/terapia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Fragmentos de Peptídeos/metabolismo
Peptidil Dipeptidase A/metabolismo
Distribuição Aleatória
Receptor Tipo 2 de Angiotensina/metabolismo
Renina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Peptide Fragments); 0 (Receptor, Angiotensin, Type 2); 30237-26-4 (Fructose); 9041-90-1 (Angiotensin I); EC 3.4.15.1 (Peptidyl-Dipeptidase A); EC 3.4.17.- (angiotensin converting enzyme 2); EC 3.4.23.15 (Renin); IJ3FUK8MOF (angiotensin I (1-7))
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170913
[St] Status:MEDLINE


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[PMID]:28874461
[Au] Autor:Shinohara K; Nakagawa P; Gomez J; Morgan DA; Littlejohn NK; Folchert MD; Weidemann BJ; Liu X; Walsh SA; Ponto LL; Rahmouni K; Grobe JL; Sigmund CD
[Ad] Endereço:From the Departments of Pharmacology (K.S., P.N., J.G., D.A.M., N.K.L., M.D.F., B.J.W., X.L., K.R., J.L.G., C.D.S.), Radiology (S.A.W., L.L.P.), and UIHC Center for Hypertension Research, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City (K.R., J.L.G., C.D.S.).
[Ti] Título:Selective Deletion of Renin-b in the Brain Alters Drinking and Metabolism.
[So] Source:Hypertension;70(5):990-997, 2017 Nov.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The brain-specific isoform of renin (Ren-b) has been proposed as a negative regulator of the brain renin-angiotensin system (RAS). We analyzed mice with a selective deletion of Ren-b which preserved expression of the classical renin (Ren-a) isoform. We reported that Ren-b mice exhibited central RAS activation and hypertension through increased expression of Ren-a, but the dipsogenic and metabolic effects in Ren-b mice are unknown. Fluid intake was similar in control and Ren-b mice at baseline and both exhibited an equivalent dipsogenic response to deoxycorticosterone acetate-salt. Dehydration promoted increased water intake in Ren-b mice, particularly after deoxycorticosterone acetate-salt. Ren-b and control mice exhibited similar body weight when fed a chow diet. However, when fed a high-fat diet, male Ren-b mice gained significantly less weight than control mice, an effect blunted in females. This difference was not because of changes in food intake, energy absorption, or physical activity. Ren-b mice exhibited increased resting metabolic rate concomitant with increased uncoupled protein 1 expression and sympathetic nerve activity to the interscapular brown adipose tissue, suggesting increased thermogenesis. Ren-b mice were modestly intolerant to glucose and had normal insulin sensitivity. Another mouse model with markedly enhanced brain RAS activity (sRA mice) exhibited pronounced insulin sensitivity concomitant with increased brown adipose tissue glucose uptake. Altogether, these data support the hypothesis that the brain RAS regulates energy homeostasis by controlling resting metabolic rate, and that Ren-b deficiency increases brain RAS activity. Thus, the relative level of expression of Ren-b and Ren-a may control activity of the brain RAS.
[Mh] Termos MeSH primário: Metabolismo Basal/fisiologia
Encéfalo/metabolismo
Hipertensão/metabolismo
Sistema Renina-Angiotensina/fisiologia
Renina/metabolismo
[Mh] Termos MeSH secundário: Animais
Ingestão de Líquidos/fisiologia
Metabolismo Energético/fisiologia
Camundongos
Isoformas de Proteínas
Sistema Nervoso Simpático/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Protein Isoforms); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170907
[St] Status:MEDLINE
[do] DOI:10.1161/HYPERTENSIONAHA.117.09923


  9 / 27530 MEDLINE  
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[PMID]:28870984
[Au] Autor:Hong AR; Kim JH; Park KS; Kim KY; Lee JH; Kong SH; Lee SY; Shin CS; Kim SW; Kim SY
[Ad] Endereço:Department of Internal MedicineSeoul National University College of Medicine, Seoul, South Korea.
[Ti] Título:Optimal follow-up strategies for adrenal incidentalomas: reappraisal of the 2016 ESE-ENSAT guidelines in real clinical practice.
[So] Source:Eur J Endocrinol;177(6):475-483, 2017 Dec.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Recently, the European Society of Endocrinology (ESE), in collaboration with the European Network for the Study of Adrenal Tumors (ENSAT), asserted that adrenal incidentalomas (AIs) <4 cm and ≤10 Hounsfield units (HU) do not require further follow-up imaging. To validate the clinical application of the follow-up strategies suggested by the 2016 ESE-ENSAT guidelines, we explored the clinical characteristics and natural course of AIs in a single center over 13 years. DESIGN AND METHODS: This retrospective cohort study included a total of 1149 patients diagnosed with AIs between 2000 and 2013 in a single tertiary center. Hormonal examination and radiological evaluations were performed at the initial diagnosis of AI and during the follow-up according to the appropriate guidelines. RESULTS: The mean age at diagnosis was 54.2 years, and the majority of AIs (68.0%) were nonfunctional lesions. Receiver operating curve analysis was used to discriminate malignant from benign lesions; the optimal cut-off value for mass size was 3.4 cm (sensitivity: 100%; specificity: 95.0%), and that for the pre-contrast HU was 19.9 (sensitivity: 100%; specificity: 67.4%). The majority of nonfunctional lesions did not change in size during the 4-year follow-up period. Applying a cut-off value of 1.8 µg/dL after a 1-mg overnight dexamethasone suppression test, 28.0% of all nonfunctional AIs progressed to autonomous cortisol secretion during the follow-up period. However, we observed no development of overt Cushing's syndrome in the study. CONCLUSIONS: We advocate that no follow-up imaging is required if the detected adrenal mass is <4 cm and has clear benign features. However, prospective studies with longer follow-up are needed to confirm the appropriate follow-up strategies.
[Mh] Termos MeSH primário: Neoplasias das Glândulas Suprarrenais/diagnóstico por imagem
Assistência ao Convalescente/métodos
[Mh] Termos MeSH secundário: Neoplasias das Glândulas Suprarrenais/sangue
Neoplasias das Glândulas Suprarrenais/diagnóstico
Neoplasias das Glândulas Suprarrenais/patologia
Neoplasias das Glândulas Suprarrenais/terapia
Adulto
Idoso
Aldosterona/sangue
Estudos de Coortes
Síndrome de Cushing/diagnóstico
Diagnóstico Diferencial
Progressão da Doença
Feminino
Seres Humanos
Hidrocortisona/sangue
Masculino
Meia-Idade
Feocromocitoma/diagnóstico
Guias de Prática Clínica como Assunto
Curva ROC
Renina/sangue
Estudos Retrospectivos
Tomografia Computadorizada por Raios X
Carga Tumoral
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
4964P6T9RB (Aldosterone); EC 3.4.23.15 (Renin); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171106
[Lr] Data última revisão:
171106
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170906
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0372


  10 / 27530 MEDLINE  
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[PMID]:28753620
[Au] Autor:Chung S; Kim S; Kim M; Koh ES; Shin SJ; Park CW; Chang YS; Kim HS
[Ad] Endereço:Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
[Ti] Título:Treatment combining aliskiren with paricalcitol is effective against progressive renal tubulointerstitial fibrosis via dual blockade of intrarenal renin.
[So] Source:PLoS One;12(7):e0181757, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to assess any potential additive effects of a treatment combining aliskiren with paricalcitol on reducing renal fibrosis. C57BL/6J mice were treated individually with aliskiren and/or paricalcitol until 7 days after initiation of unilateral ureteral obstruction (UUO).In obstructed kidneys of UUO mice, monotherapy with aliskiren or paricalcitol significantly attenuated interstitial fibrosis, collagen IV accumulation, and α-smooth muscle actin- and terminal deoxynucleotidyl transferase-mediated biotin nick end-labeling-positive cells. The combination treatment showed additive efficacy in inhibition of these parameters. Renal NADPH oxidase (Nox)1 and Nox2 were significantly decreased by aliskiren or paricalcitol alone or in combination, while renal Nox4 expression was significantly reduced by paricalcitol mono- or combination treatment. Increased levels of p-Erk and p-p38 MAPK, and NF-κB in UUO kidneys were also significantly reduced by either aliskiren or paricalcitol treatment alone or in combination. Aliskiren or paricalcitol monotherapy significantly reduced the expression of (pro)renin receptor in UUO kidneys. In addition, aliskiren tended to augment renin expression in UUO kidneys, but paricalcitol reduced its expression level. The combination treatment effectively blocked both (pro)renin receptor and renin expression induced by aliskiren, and resulted in a further reduction of the renal expression of angiotensin II AT1 receptor. Aliskiren failed to increase the expression of vitamin D receptor in UUO kidneys, but the combination treatment restored its expression level. Taken together, a treatment combining aliskiren with paricalcitol better inhibits UUO-induced renal injury. The mechanism of this synergy may involve more profound inhibition of the intrarenal renin-angiotensin system.
[Mh] Termos MeSH primário: Amidas/uso terapêutico
Progressão da Doença
Ergocalciferóis/uso terapêutico
Fumaratos/uso terapêutico
Nefropatias/tratamento farmacológico
Rim/metabolismo
Renina/metabolismo
[Mh] Termos MeSH secundário: Amidas/farmacologia
Animais
Apoptose/efeitos dos fármacos
Colágeno Tipo IV/metabolismo
Quimioterapia Combinada
Ergocalciferóis/farmacologia
Fibrose
Fumaratos/farmacologia
Mediadores da Inflamação/metabolismo
Nefropatias/patologia
Masculino
Camundongos Endogâmicos C57BL
Miofibroblastos/efeitos dos fármacos
Miofibroblastos/metabolismo
Estresse Oxidativo/efeitos dos fármacos
Receptores de Calcitriol/metabolismo
Sistema Renina-Angiotensina/efeitos dos fármacos
Resultado do Tratamento
Obstrução Ureteral/tratamento farmacológico
Obstrução Ureteral/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amides); 0 (Collagen Type IV); 0 (Ergocalciferols); 0 (Fumarates); 0 (Inflammation Mediators); 0 (Receptors, Calcitriol); 502FWN4Q32 (aliskiren); 6702D36OG5 (paricalcitol); EC 3.4.23.15 (Renin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170729
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0181757



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