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[PMID]:28454724
[Au] Autor:Nagarajan S; Vohra T; Loffing J; Faresse N
[Ad] Endereço:Institute of Anatomy, University of Zurich, 8057 Zurich, Switzerland; National Center of Competence in Research "Kidney.CH", Switzerland.
[Ti] Título:Protein Phosphatase 1α enhances renal aldosterone signaling via mineralocorticoid receptor stabilization.
[So] Source:Mol Cell Endocrinol;450:74-82, 2017 Jul 15.
[Is] ISSN:1872-8057
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Stimulation of the mineralocorticoid receptor (MR) by aldosterone controls several physiological parameters including blood pressure, inflammation or metabolism. We previously showed that MR turnover constitutes a crucial regulatory step in the responses of renal epithelial cells to aldosterone. Here, we identified Protein Phosphatase 1 alpha (PP1α), as a novel cytoplasmic binding partner of MR that promotes the receptor activity. The RT-PCR expression mapping of PP1α reveals a high expression in the kidney, particularly in the distal part of the nephron. At the molecular level, we demonstrate that PP1α inhibits the ubiquitin ligase Mdm2 by dephosphorylation, preventing its interaction with MR. This results in the accumulation of the receptor due to reduction of its proteasomal degradation and consequently a greater aldosterone-induced Na uptake by renal cells. Thus, our findings describe an original mechanism involving a phosphatase in the regulation of aldosterone signaling and provide new and important insights into the molecular mechanism underlying the MR turnover.
[Mh] Termos MeSH primário: Aldosterona/metabolismo
Rim/metabolismo
Proteína Fosfatase 1/metabolismo
Receptores de Mineralocorticoides/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Células Epiteliais/efeitos dos fármacos
Células Epiteliais/metabolismo
Células HEK293
Seres Humanos
Camundongos Endogâmicos C57BL
Complexo de Endopeptidases do Proteassoma/metabolismo
Ligação Proteica/efeitos dos fármacos
Domínios Proteicos
Estabilidade Proteica/efeitos dos fármacos
Proteólise/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-mdm2/metabolismo
Receptores de Mineralocorticoides/química
Transdução de Sinais/efeitos dos fármacos
Sódio/metabolismo
Transcrição Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Mineralocorticoid); 4964P6T9RB (Aldosterone); 9NEZ333N27 (Sodium); EC 2.3.2.27 (Proto-Oncogene Proteins c-mdm2); EC 3.1.3.16 (Protein Phosphatase 1); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[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:170430
[St] Status:MEDLINE


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[PMID]:29348113
[Au] Autor:Monticone S; Buffolo F; Tetti M; Veglio F; Pasini B; Mulatero P
[Ad] Endereço:Division of Internal Medicine and Hypertension UnitDepartment of Medical Sciences, University of Torino, Torino, Italy.
[Ti] Título:GENETICS IN ENDOCRINOLOGY: The expanding genetic horizon of primary aldosteronism.
[So] Source:Eur J Endocrinol;178(3):R101-R111, 2018 Mar.
[Is] ISSN:1479-683X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aldosterone is the main mineralocorticoid hormone in humans and plays a key role in maintaining water and electrolyte homeostasis. Primary aldosteronism (PA), characterized by autonomous aldosterone overproduction by the adrenal glands, affects 6% of the general hypertensive population and can be either sporadic or familial. Aldosterone-producing adenoma (APA) and bilateral adrenal hyperplasia (BAH) are the two most frequent subtypes of sporadic PA and 4 forms of familial hyperaldosteronism (FH-I to FH-IV) have been identified. Over the last six years, the introduction of next-generation sequencing has significantly improved our understanding of the molecular mechanisms responsible for autonomous aldosterone overproduction in both sporadic and familial PA. Somatic mutations in four genes ( and ), differently implicated in intracellular ion homeostasis, have been identified in nearly 60% of the sporadic APAs. Germline mutations in and cause FH-III and FH-IV, respectively, while germline mutations in cause the rare PASNA syndrome, featuring primary aldosteronism seizures and neurological abnormalities. Further studies are warranted to identify the molecular mechanisms underlying BAH and FH-II, the most common forms of sporadic and familial PA whose molecular basis is yet to be uncovered.
[Mh] Termos MeSH primário: Canais de Cálcio Tipo L/genética
Canais de Potássio Corretores do Fluxo de Internalização Acoplados a Proteínas G/genética
Hiperaldosteronismo/genética
ATPases Transportadoras de Cálcio da Membrana Plasmática/genética
ATPase Trocadora de Sódio-Potássio/genética
[Mh] Termos MeSH secundário: Aldosterona/biossíntese
Variação Genética
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (CACNA1D protein, human); 0 (Calcium Channels, L-Type); 0 (G Protein-Coupled Inwardly-Rectifying Potassium Channels); 0 (KCNJ5 protein, human); 4964P6T9RB (Aldosterone); EC 3.6.1.- (ATP1A1 protein, human); EC 3.6.3.8 (ATP2B3 protein, human); EC 3.6.3.8 (Plasma Membrane Calcium-Transporting ATPases); EC 3.6.3.9 (Sodium-Potassium-Exchanging ATPase)
[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:180120
[St] Status:MEDLINE
[do] DOI:10.1530/EJE-17-0946


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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]:28468286
[Au] Autor:Inoue K; Omura M; Sugisawa C; Tsurutani Y; Saito J; Nishikawa T
[Ad] Endereço:Endocrinology and Diabetes Center, Yokohama Rosai Hospital, Yokohama 222-0036, Japan. koinoue-tky@umin.ac.jp.
[Ti] Título:Clinical Utility of the Adrenocorticotropin Stimulation Test with/without Dexamethasone Suppression for Definitive and Subtype Diagnosis of Primary Aldosteronism.
[So] Source:Int J Mol Sci;18(5), 2017 Apr 30.
[Is] ISSN:1422-0067
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:The adrenocorticotropin (ACTH) stimulation test (AST) has been reported to be useful for diagnosing primary aldosteronism (PA), particularly for differentiating PA subtypes under 1-mg dexamethasone suppression (DS). The aim of our study was to clarify the effect of 1-mg DS on AST results. A retrospective cohort study was conducted using data for 48 patients (PA: 30/48). We estimated the difference in plasma aldosterone concentration (PAC) responsiveness to ACTH stimulation with single (AST alone) and combined (AST under 1-mg DS) tests within the same patient. We compared the diagnostic accuracy of these two tests for PA and the laterality of hyperaldosteronism. We found no differences in PAC responsiveness to ACTH stimulation between single and combined tests, and observed a significant positive linear relationship (30 min, ² = 0.75, -value < 0.01). Both tests showed the highest diagnostic accuracy for PA following 30 min of ACTH stimulation. The ability to detect the laterality of hyperaldosteronism was inconsistent and differed according to the two definitions: lateralization ratio and the absolute aldosterone levels in adrenal venous sampling. PAC responsiveness to ACTH stimulation was similar for AST with and without 1-mg DS. AST can be performed under both conditions with similar accuracy to detect PA.
[Mh] Termos MeSH primário: Testes de Função do Córtex Suprarrenal/métodos
Hormônio Adrenocorticotrópico/administração & dosagem
Aldosterona/sangue
Dexametasona/administração & dosagem
Hiperaldosteronismo/sangue
[Mh] Termos MeSH secundário: Testes de Função do Córtex Suprarrenal/normas
Adulto
Feminino
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
4964P6T9RB (Aldosterone); 7S5I7G3JQL (Dexamethasone); 9002-60-2 (Adrenocorticotropic Hormone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE


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[PMID]:28744670
[Au] Autor:Lema I; Amazit L; Lamribet K; Fagart J; Blanchard A; Lombès M; Cherradi N; Viengchareun S
[Ad] Endereço:Inserm U1185, Faculté de Médecine Paris-Sud, Université Paris-Saclay, 63 rue Gabriel Peri, 94276, Le Kremlin-Bicêtre, France.
[Ti] Título:RNA-binding protein HuR enhances mineralocorticoid signaling in renal KC3AC1 cells under hypotonicity.
[So] Source:Cell Mol Life Sci;74(24):4587-4597, 2017 12.
[Is] ISSN:1420-9071
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Mineralocorticoid receptor (MR) mediates the sodium-retaining action of aldosterone in the distal nephron. Herein, we decipher mechanisms by which hypotonicity increases MR expression in renal principal cells. We identify HuR (human antigen R), an mRNA-stabilizing protein, as an important posttranscriptional regulator of MR expression. Hypotonicity triggers a rapid and reversible nuclear export of HuR in renal KC3AC1 cells, as quantified by high-throughput microscopy. We also identify a key hairpin motif in the 3'-untranslated region of MR transcript, pivotal for the interaction with HuR and its stabilizing function. Next, we show that hypotonicity increases MR recruitment onto Sgk1 promoter, a well-known MR target gene, thereby enhancing aldosterone responsiveness. Our data shed new light on the crucial role of HuR as a stabilizing factor for the MR transcript and provide evidence for a short autoregulatory loop in which expression of a nuclear receptor transcriptionally regulating water and sodium balance is controlled by osmotic tone.
[Mh] Termos MeSH primário: Proteína Semelhante a ELAV 1/metabolismo
Rim/metabolismo
Mineralocorticoides/metabolismo
Pressão Osmótica/fisiologia
Proteínas de Ligação a RNA/metabolismo
Receptores de Mineralocorticoides/metabolismo
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas/genética
Transporte Ativo do Núcleo Celular/genética
Aldosterona/metabolismo
Regulação da Expressão Gênica/genética
Células HEK293
Seres Humanos
Proteínas Imediatamente Precoces/metabolismo
Rim/fisiologia
Osmose/fisiologia
Regiões Promotoras Genéticas/genética
Proteínas Serina-Treonina Quinases/metabolismo
Processamento Pós-Transcricional do RNA/genética
RNA Mensageiro/metabolismo
Transcrição Genética/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (ELAV-Like Protein 1); 0 (ELAVL1 protein, human); 0 (Immediate-Early Proteins); 0 (Mineralocorticoids); 0 (RNA, Messenger); 0 (RNA-Binding Proteins); 0 (Receptors, Mineralocorticoid); 4964P6T9RB (Aldosterone); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (serum-glucocorticoid regulated kinase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1007/s00018-017-2594-x


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[PMID]:28454766
[Au] Autor:Rieke S; Heise T; Schmidt F; Haider W; Bednarz H; Niehaus K; Mentz A; Kalinowski J; Hirsch-Ernst KI; Steinberg P; Niemann L; Marx-Stoelting P
[Ad] Endereço:Bundesinstitut für Risikobewertung (BfR), Department for Pesticides Safety, Max-Dohrn-Str. 8-10, 10589 Berlin, Germany.
[Ti] Título:Mixture effects of azole fungicides on the adrenal gland in a broad dose range.
[So] Source:Toxicology;385:28-37, 2017 06 15.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Consumers are exposed to low concentrations of a variety of pesticide residues in or on food. Some of them might interfere with the endocrine system. While each individual active substance has been extensively tested for toxicity and safety, potential combination effects possibly resulting from combined exposure to different pesticides have seldomly been tested so far, especially in vivo. Since the adrenal gland is a key endocrine organ, we investigated if and how substances of a group of fungicides presumed to interfere with the biosynthesis of steroid hormones affect this organ when applied individually and in combination in a broad dose range. A 28-day feeding study was conducted in Wistar rats by using three (tri)azole fungicides considered to potentially affect the endocrine system (cyproconazole, epoxiconazole and prochloraz) individually at five dose levels, ranging from 0.9ppm to 2400ppm, and in combination at three dose levels. The parameters analysed included classical toxicology (pathology, histopathology, clinical chemistry) and molecular toxicology endpoints (gene expression arrays and quantitative real time PCR e.g. of Star, HSD3ß, Cyp11a1, Cyp11b1, Cyp11b2, Cyp 21, ApoE), as well as hormone analysis. A dose-dependent decrease in the adrenal gland weight of rats treated with epoxiconazole alone, which was accompanied by an atrophy of the adrenal gland as well as by an increase in the serum cholesterol level and which only became statistically significant at the top dose levels, was observed. These effects were attenuated in the combination experiments, although the same epoxiconazole concentration was used.
[Mh] Termos MeSH primário: Glândulas Suprarrenais/efeitos dos fármacos
Azóis/toxicidade
Fungicidas Industriais/toxicidade
[Mh] Termos MeSH secundário: 3-Hidroxiesteroide Desidrogenases/genética
Glândulas Suprarrenais/metabolismo
Glândulas Suprarrenais/patologia
Aldosterona/sangue
Animais
Apolipoproteínas E/genética
Colesterol/sangue
Corticosterona/sangue
Sistema Enzimático do Citocromo P-450/genética
Interações Medicamentosas
Expressão Gênica/efeitos dos fármacos
Masculino
Nível de Efeito Adverso não Observado
Tamanho do Órgão/efeitos dos fármacos
Fosfoproteínas/genética
Progesterona/sangue
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Azoles); 0 (Fungicides, Industrial); 0 (Phosphoproteins); 0 (steroidogenic acute regulatory protein); 4964P6T9RB (Aldosterone); 4G7DS2Q64Y (Progesterone); 9035-51-2 (Cytochrome P-450 Enzyme System); 97C5T2UQ7J (Cholesterol); EC 1.1.- (3-Hydroxysteroid Dehydrogenases); W980KJ009P (Corticosterone)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180122
[Lr] Data última revisão:
180122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE


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[PMID]:27777363
[Au] Autor:Zhou J; Lam B; Neogi SG; Yeo GS; Azizan EA; Brown MJ
[Ad] Endereço:From the Centre for Clinical Pharmacology, William Harvey Research Institute, Barts and the London School of Medicine & Dentistry, Queen Mary University of London, United Kingdom (J.Z., M.J.B.); Clinical Pharmacology Unit, Department of Medicine, University of Cambridge (J.Z.), University of Cam
[Ti] Título:Transcriptome Pathway Analysis of Pathological and Physiological Aldosterone-Producing Human Tissues.
[So] Source:Hypertension;68(6):1424-1431, 2016 12.
[Is] ISSN:1524-4563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Primary aldosteronism is present in ≈10% of hypertensives. We previously performed a microarray assay on aldosterone-producing adenomas and their paired zona glomerulosa and fasciculata. Confirmation of top genes validated the study design and functional experiments of zona glomerulosa selective genes established the role of the encoded proteins in aldosterone regulation. In this study, we further analyzed our microarray data using AmiGO 2 for gene ontology enrichment and Ingenuity Pathway Analysis to identify potential biological processes and canonical pathways involved in pathological and physiological aldosterone regulation. Genes differentially regulated in aldosterone-producing adenoma and zona glomerulosa were associated with steroid metabolic processes gene ontology terms. Terms related to the Wnt signaling pathway were enriched in zona glomerulosa only. Ingenuity Pathway Analysis showed "NRF2-mediated oxidative stress response pathway" and "LPS (lipopolysaccharide)/IL-1 (interleukin-1)-mediated inhibition of RXR (retinoid X receptor) function" were affected in both aldosterone-producing adenoma and zona glomerulosa with associated genes having up to 21- and 8-fold differences, respectively. Comparing KCNJ5-mutant aldosterone-producing adenoma, zona glomerulosa, and zona fasciculata samples with wild-type samples, 138, 56, and 59 genes were differentially expressed, respectively (fold-change >2; P<0.05). ACSS3, encoding the enzyme that synthesizes acetyl-CoA, was the top gene upregulated in KCNJ5-mutant aldosterone-producing adenoma compared with wild-type. NEFM, a gene highly upregulated in zona glomerulosa, was upregulated in KCNJ5 wild-type aldosterone-producing adenomas. NR4A2, the transcription factor for aldosterone synthase, was highly expressed in zona fasciculata adjacent to a KCNJ5-mutant aldosterone-producing adenoma. Further interrogation of these genes and pathways could potentially provide further insights into the pathology of primary aldosteronism.
[Mh] Termos MeSH primário: Adenoma/genética
Aldosterona/metabolismo
Canais de Potássio Corretores do Fluxo de Internalização Acoplados a Proteínas G/genética
Hiperaldosteronismo/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Adenoma/fisiopatologia
Córtex Suprarrenal/patologia
Córtex Suprarrenal/fisiologia
Perfilação da Expressão Gênica
Regulação da Expressão Gênica
Seres Humanos
Hiperaldosteronismo/fisiopatologia
Feocromocitoma/genética
Feocromocitoma/fisiopatologia
Amostragem
Regulação para Cima
Via de Sinalização Wnt
Zona Fasciculada/metabolismo
Zona Glomerulosa/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (G Protein-Coupled Inwardly-Rectifying Potassium Channels); 0 (KCNJ5 protein, human); 0 (Transcription Factors); 4964P6T9RB (Aldosterone)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE


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[PMID]:29220406
[Au] Autor:Okamoto C; Hayakawa Y; Aoyama T; Komaki H; Minatoguchi S; Iwasa M; Yamada Y; Kanamori H; Kawasaki M; Nishigaki K; Mikami A; Minatoguchi S
[Ad] Endereço:Department of Cardiology, Gifu University Graduate School of Medicine, Yanagido, Gifu, Japan.
[Ti] Título:Excessively low salt diet damages the heart through activation of cardiac (pro) renin receptor, renin-angiotensin-aldosterone, and sympatho-adrenal systems in spontaneously hypertensive rats.
[So] Source:PLoS One;12(12):e0189099, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: A high salt intake causes hypertension and leads to cardiovascular disease. Therefore, a low salt diet is now recommended to prevent hypertension and cardiovascular disease. However, it is still unknown whether an excessively low salt diet is beneficial or harmful for the heart. METHODS: Wistar Kyoto rats (WKYs) and spontaneously hypertensive rats (SHRs) received normal salt chow (0.9% salt diet) and excessively low salt chow (0.01% salt diet referred to as saltless diet) for 8 weeks from 8 to 16 weeks of age. The effects of the excessively low salt diet on the cardiac (pro) renin receptor, renin-angiotensin-aldosterone, and sympatho-adrenal systems were investigated. RESULTS: The excessively low salt diet did not affect the systolic blood pressure but significantly increased the heart rate both in WKYs and SHRs. The excessively low salt diet significantly elevated plasma renin activity, plasma angiotensin I, II and aldosterone concentrations, and plasma noradrenaline and adrenaline concentrations both in WKYs and SHRs. Cardiac expressions of renin, prorenin, (P)RR, angiotensinogen, and angiotensin II AT1 receptor and phosphorylated (p)-ERK1/2, p-HSP27, p-38MAPK, and TGF-ß1 were significantly enhanced by the excessively low salt diet in both WKYs and SHRs. The excessively low salt diet accelerated cardiac interstitial and perivascular fibrosis and increased the cardiomyocyte size and interventricular septum thickness in WKYs and SHRs but the extent was greater in SHRs. CONCLUSION: An excessively low salt diet damages the heart through activation of plasma renin-angiotensin-aldosterone and sympatho-adrenal systems and activation of cardiac (P)RR and angiotensin II AT1 receptor and their downstream signals both in WKYs and SHRs.
[Mh] Termos MeSH primário: Aldosterona/metabolismo
Dieta Hipossódica/efeitos adversos
Coração/fisiopatologia
Receptores de Superfície Celular/agonistas
Sistema Renina-Angiotensina/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Ratos
Ratos Endogâmicos SHR
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Cell Surface); 0 (prorenin receptor); 4964P6T9RB (Aldosterone)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189099


  9 / 21294 MEDLINE  
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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]:28970286
[Au] Autor:Werth S; Müller-Fielitz H; Raasch W
[Ad] Endereço:Institute of Experimental and Clinical Pharmacology and ToxicologyUniversity of Lübeck, Lübeck, Germany.
[Ti] Título:Obesity-stimulated aldosterone release is not related to an S1P-dependent mechanism.
[So] Source:J Endocrinol;235(3):251-265, 2017 Dec.
[Is] ISSN:1479-6805
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Aldosterone has been identified as an important factor in obesity-associated hypertension. Here, we investigated whether sphingosine-1-phosphate (S1P), which has previously been linked to obesity, increases aldosterone release. S1P-induced aldosterone release was determined in NCI H295R cells in the presence of S1P receptor (S1PR) antagonists. release of S1P (100-300 µg/kg ) was investigated in pithed, lean Sprague Dawley (SD) rats, diet-obese spontaneous hypertensive rats (SHRs), as well as in lean or obese Zucker rats. Aldosterone secretion was increased in NCI H295R cells by S1P, the selective S1PR1 agonist SEW2871 and the selective S1PR2 antagonist JTE013. Treatment with the S1PR1 antagonist W146 or fingolimod and the S1PR1/3 antagonist VPbib2319 decreased baseline and/or S1P-stimulated aldosterone release. Compared to saline-treated SD rats, plasma aldosterone increased by ~50 pg/mL after infusing S1P. Baseline levels of S1P and aldosterone were higher in obese than in lean SHRs. Adrenal S1PR expression did not differ between chow- or CD-fed rats that had the highest S1PR1 and lowest S1PR4 levels. S1P induced a short-lasting increase in plasma aldosterone in obese, but not in lean SHRs. However, 2-ANOVA did not demonstrate any difference between lean and obese rats. S1P-induced aldosterone release was also similar between obese and lean Zucker rats. We conclude that S1P is a local regulator of aldosterone production. S1PR1 agonism induces an increase in aldosterone secretion, while stimulating adrenal S1PR2 receptor suppresses aldosterone production. A significant role of S1P in influencing aldosterone secretion in states of obesity seems unlikely.
[Mh] Termos MeSH primário: Aldosterona/metabolismo
Lisofosfolipídeos/fisiologia
Obesidade/metabolismo
Receptores de Lisoesfingolipídeo/fisiologia
Esfingosina/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Dieta Hiperlipídica
Seres Humanos
Lisofosfolipídeos/metabolismo
Masculino
Obesidade/sangue
Obesidade/etiologia
Ratos
Ratos Endogâmicos SHR
Ratos Sprague-Dawley
Ratos Zucker
Receptores de Lisoesfingolipídeo/metabolismo
Transdução de Sinais/fisiologia
Esfingosina/metabolismo
Esfingosina/fisiologia
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lysophospholipids); 0 (Receptors, Lysosphingolipid); 26993-30-6 (sphingosine 1-phosphate); 4964P6T9RB (Aldosterone); NGZ37HRE42 (Sphingosine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171004
[St] Status:MEDLINE
[do] DOI:10.1530/JOE-16-0550



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