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[PMID]:28456775
[Au] Autor:Bartus K; Podolec J; Lee RJ; Kapelak B; Sadowski J; Bartus M; Oles K; Ceranowicz P; Trabka R; Litwinowicz R
[Ad] Endereço:Department of Cardiovascular Surgery and Transplantology, Jagiellonian University, Collegium Medicum, John Paul II Hospital, Cracow, Poland.
[Ti] Título:Atrial natriuretic peptide and brain natriuretic peptide changes after epicardial percutaneous left atrial appendage suture ligation using LARIAT device.
[So] Source:J Physiol Pharmacol;68(1):117-123, 2017 Feb.
[Is] ISSN:1899-1505
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Percutaneous left atrial appendage closure is an alternative treatment for stroke and systemic thromboembolism risk reduction in non-valvular atrial fibrillation (AF). However, the neurohormonal impact of epicardial exclusion of the left atrial appendage (LAA) with the LARIAT procedure is unknown. Evaluation of changes in atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) levels in AF patients underwent percutaneous LAA suture ligation. Sixty six patients underwent successfully percutaneous LAA suture ligation using LARIAT device. The level of ANP and BNP was measured before and 3 months after procedure. Mean ANP level before procedure was 249 ± 77 pg/mL (range from 95 pg/mL to 503 pg/mL) and mean BNP level was 481 ± 517 pg/mL (range from 34 pg/mL to 2508 pg/mL). Three months after procedure mean ANP level was 249 ± 79 pg/mL (range from 98 pg/mL to 492 pg/mL) and mean BNP level was 495 ± 526 pg/mL (range from 52 pg/mL to 2420 pg/mL). At 3 months follow up after percutaneous LAA suture ligation there were no significant differences in ANP and BNP levels.
[Mh] Termos MeSH primário: Apêndice Atrial/cirurgia
Fibrilação Atrial/cirurgia
Fator Natriurético Atrial/sangue
Ligadura/instrumentação
Peptídeo Natriurético Encefálico/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Fibrilação Atrial/sangue
Feminino
Seres Humanos
Masculino
Meia-Idade
Suturas
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE
[Nm] Nome de substância:
114471-18-0 (Natriuretic Peptide, Brain); 85637-73-6 (Atrial Natriuretic Factor)
[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:170501
[St] Status:MEDLINE


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[PMID]:29279524
[Au] Autor:Li X; Liang Y; Qiao Z; Yang J; Han P; Zhao B; Li F; Lv H; Guo J; Gao F; Li L
[Ad] Endereço:Department of Cardiology, Hongqi Hospital, Mudanjiang Medical College.
[Ti] Título:Transcriptional Analysis of Endothelial Cell Alternation Induced by Atrial Natriuretic Polypeptide in Human Umbilical Vein Endothelial Cells.
[So] Source:Int Heart J;59(1):197-202, 2018 Jan 27.
[Is] ISSN:1349-3299
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The aim of this study was to explore how atrial natriuretic polypeptide (ANP) affects the properties and function of endothelial cells. Gene expression data GSE56976 generated at 0, 1, and 6 hours after ANP incubation in human umbilical vein endothelial cells (HUVEC) was used. Microarray data were preprocessed for differentially expressed genes (DEGs) in each time-dependent group. Next, gene ontology (GO), pathway analysis, and transcriptional regulation were performed. Co-expression clustering analysis of DEGs and functional enrichment analysis of co-expression modules were processed. RT-PCR analysis was performed to validate gene expression. DEGs were obtained and their counts were increased from 0 hours to 6 hours. No overlapping DEGs were obtained among the 3 groups. The DEGs of ANP_6hours, including TGFB2 (transforming growth factor, beta 2), LTF (lactotransferrin/lactoferrin), and ETV7 (Ets variant 7) were mainly related with cell apoptosis and immune responses. The DEGs in the network of ANP_0hour were mainly associated with epithelial ion transport processes. In addition, 3 co-expressed modules were detected. CSF2 (colony stimulating factor 2) and PF4 (platelet factor 4) of the blue module were related with cytolysis, while FXYD1 (FXYD domain containing ion transport regulator 1) and TGFB2 of the yellow module were mainly enriched in ion transport and the ovulation cycle. The expression of TGFB2 obtained by microarray analysis was consistent with that of RT-PCR. Ion transport could be affected promptly after ANP treatment, and subsequently, the cytolysis of vein endothelial cells may be promoted and endothelial permeability would be enhanced, followed by activated immune responses.
[Mh] Termos MeSH primário: Apoptose
Fator Natriurético Atrial/farmacologia
Regulação da Expressão Gênica
Células Endoteliais da Veia Umbilical Humana/metabolismo
Lactoferrina/genética
Proteínas Proto-Oncogênicas c-ets/genética
Fator de Crescimento Transformador beta2/genética
[Mh] Termos MeSH secundário: Células Cultivadas
Perfilação da Expressão Gênica
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/patologia
Seres Humanos
Lactoferrina/biossíntese
Proteínas Proto-Oncogênicas c-ets/biossíntese
RNA/genética
Reação em Cadeia da Polimerase em Tempo Real
Fator de Crescimento Transformador beta2/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ETV7 protein, human); 0 (LTF protein, human); 0 (Proto-Oncogene Proteins c-ets); 0 (TGFB2 protein, human); 0 (Transforming Growth Factor beta2); 63231-63-0 (RNA); 85637-73-6 (Atrial Natriuretic Factor); EC 3.4.21.- (Lactoferrin)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180206
[Lr] Data última revisão:
180206
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1536/ihj.16-522


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Resende, Elmiro Santos
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[PMID]:28452559
[Au] Autor:Roever L; Resende ES; Roerver-Borges AS
[Ad] Endereço:1 Federal University of Uberlândia, Department of Clinical Research, Uberlândia, Brazil.
[Ti] Título:Impact of pro-atrial natriuretic peptide in atrial fibrillation and stroke.
[So] Source:Eur J Prev Cardiol;24(12):1239-1241, 2017 08.
[Is] ISSN:2047-4881
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Fibrilação Atrial
Fator Natriurético Atrial
[Mh] Termos MeSH secundário: Biomarcadores
Seres Humanos
Peptídeo Natriurético Encefálico
Fragmentos de Peptídeos
Acidente Vascular Cerebral
[Pt] Tipo de publicação:EDITORIAL; COMMENT
[Nm] Nome de substância:
0 (Biomarkers); 0 (Peptide Fragments); 114471-18-0 (Natriuretic Peptide, Brain); 85637-73-6 (Atrial Natriuretic Factor)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1177/2047487317707832


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[PMID]:29253899
[Au] Autor:Cannone V; Scott CG; Decker PA; Larson NB; Palmas W; Taylor KD; Wang TJ; Gupta DK; Bielinski SJ; Burnett JC
[Ad] Endereço:Cardiorenal Research Laboratory, Mayo Clinic, Rochester, Minnesota, United States of America.
[Ti] Título:A favorable cardiometabolic profile is associated with the G allele of the genetic variant rs5068 in African Americans: The Multi-Ethnic Study of Atherosclerosis (MESA).
[So] Source:PLoS One;12(12):e0189858, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In whites, the minor G allele of the atrial natriuretic peptide (ANP) genetic variant rs5068 is associated with higher circulating levels of ANP and B-type natriuretic peptide (BNP), lower risk of hypertension, higher high-density lipoprotein (HDL) cholesterol plasma levels, and lower prevalence of obesity and metabolic syndrome. The observed phenotype is consistent with the blood pressure lowering and metabolic properties of ANP and BNP. The cardiovascular and metabolic phenotype associated with rs5068 genotypes in African Americans is undefined. We genotyped 1631 African Americans in the Multi-Ethnic Study of Atherosclerosis (MESA) for rs5068 and investigated their phenotype. Genotype frequencies of rs5068 were 93.2% AA (n = 1520), 6.7% AG (n = 110) and 0.1% GG (n = 1). All subsequent analyses are AG + GG versus AA genotype. Using a Bonferroni corrected level of significance of 0.005, the prevalence of metabolic syndrome (23% vs 38%, age-sex-adjusted p = 0.002) and triglycerides plasma values (76 vs 90 mg/dl, age-sex-BMI adjusted p = 0.004) were both significantly lower in the AG+GG genotypes. In the AG+GG genotypes, the prevalence of diabetes (8% vs 18%, age-sex-BMI-adjusted p = 0.02) and insulin plasma levels tended to be lower (4.8 vs 5.7 µU/ml, age-sex-BMI adjusted p = 0.04) whereas HDL-cholesterol levels tended to be higher (55 vs 50 mg/dl, age-sex-BMI-adjusted p = 0.04). No association was found with hypertension. The association between the rs5068 G allele and a favorable metabolic phenotype is now shown in African Americans. The rs5068 AG+GG genotypes are associated with lower prevalence of metabolic syndrome and lower triglycerides values.
[Mh] Termos MeSH primário: Aterosclerose/etnologia
Aterosclerose/genética
Fator Natriurético Atrial/genética
Doenças Cardiovasculares/etnologia
Doenças Cardiovasculares/genética
Doenças Cardiovasculares/prevenção & controle
[Mh] Termos MeSH secundário: Afroamericanos
Idoso
Idoso de 80 Anos ou mais
Alelos
Sistema Cardiovascular
HDL-Colesterol/sangue
Estudos de Coortes
Grupos Étnicos
Feminino
Genótipo
Geografia
Seres Humanos
Insulina/sangue
Masculino
Síndrome Metabólica/sangue
Meia-Idade
Peptídeo Natriurético Encefálico/sangue
Obesidade/sangue
Obesidade/genética
Fenótipo
Prevalência
Triglicerídeos/sangue
Estados Unidos
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Cholesterol, HDL); 0 (Insulin); 0 (Triglycerides); 114471-18-0 (Natriuretic Peptide, Brain); 85637-73-6 (Atrial Natriuretic Factor)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189858


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[PMID]:28911179
[Au] Autor:Seron-Ferre M; Torres-Farfan C; Valenzuela FJ; Castillo-Galan S; Rojas A; Mendez N; Reynolds H; Valenzuela GJ; Llanos AJ
[Ad] Endereço:Laboratorio de Cronobiología, Universidad de Chile, Santiago 16038, Chile.
[Ti] Título:Deciphering the Function of the Blunt Circadian Rhythm of Melatonin in the Newborn Lamb: Impact on Adrenal and Heart.
[So] Source:Endocrinology;158(9):2895-2905, 2017 Sep 01.
[Is] ISSN:1945-7170
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neonatal lambs, as with human and other neonates, have low arrhythmic endogenous levels of melatonin for several weeks until they start their own pineal rhythm of melatonin production at approximately 2 weeks of life. During pregnancy, daily rhythmic transfer of maternal melatonin to the fetus has important physiological roles in sheep, nonhuman primates, and rats. This melatonin rhythm provides a circadian signal and also participates in adjusting the physiology of several organs in preparation for extrauterine life. We propose that the ensuing absence of a melatonin rhythm plays a role in neonatal adaptation. To test this hypothesis, we studied the effects of imposing a high-amplitude melatonin rhythm in the newborn lamb on (1) clock time-related changes in cortisol and plasma variables and (2) clock time-related changes of gene expression of clock genes and selected functional genes in the adrenal gland and heart. We treated newborn lambs with a daily oral dose of melatonin (0.25 mg/kg) from birth to 5 days of age, recreating a high-amplitude melatonin rhythm. This treatment suppressed clock time-related changes of plasma adrenocorticotropic hormone, cortisol, clock gene expression, and functional genes in the newborn adrenal gland. In the heart, it decreased heart/body weight ratio, increased expression of Anp and Bnp, and resulted in different heart gene expression from control newborns. The interference of this postnatal melatonin treatment with the normal postnatal pattern of adrenocortical function and heart development support a physiological role for the window of flat postnatal melatonin levels during the neonatal transition.
[Mh] Termos MeSH primário: Glândulas Suprarrenais/metabolismo
Ritmo Circadiano/fisiologia
Melatonina/sangue
Miocárdio/metabolismo
[Mh] Termos MeSH secundário: Glândulas Suprarrenais/efeitos dos fármacos
Animais
Animais Recém-Nascidos
Fator Natriurético Atrial/genética
Fator Natriurético Atrial/metabolismo
Feminino
Expressão Gênica/efeitos dos fármacos
Coração/efeitos dos fármacos
Coração/fisiologia
Masculino
Melatonina/farmacologia
Melatonina/fisiologia
Peptídeo Natriurético Encefálico/genética
Proteínas Circadianas Period/genética
Ovinos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Period Circadian Proteins); 114471-18-0 (Natriuretic Peptide, Brain); 85637-73-6 (Atrial Natriuretic Factor); JL5DK93RCL (Melatonin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE
[do] DOI:10.1210/en.2017-00254


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[PMID]:28822817
[Au] Autor:Pharaon LF; El-Orabi NF; Kunhi M; Al Yacoub N; Awad SM; Poizat C
[Ad] Endereço:King Saud University, College of Pharmacy, Department of Pharmacology and Toxicology, PO Box 22452, Riyadh 11495, Saudi Arabia; Cardiovascular Research Program, King Faisal Specialist Hospital & Research Centre, PO Box 3354, Riyadh 11211, Saudi Arabia.
[Ti] Título:Rosiglitazone promotes cardiac hypertrophy and alters chromatin remodeling in isolated cardiomyocytes.
[So] Source:Toxicol Lett;280:151-158, 2017 Oct 05.
[Is] ISSN:1879-3169
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Rosiglitazone is an anti-diabetic agent that raised a major controversy over its cardiovascular adverse effects. There is in vivo evidence that Rosiglitazone promotes cardiac hypertrophy by PPAR-γ-independent mechanisms. However, whether Rosiglitazone directly alters hypertrophic growth in cardiac cells is unknown. Chromatin remodeling by histone post-translational modifications has emerged as critical for many cardiomyopathies. Based on these observations, this study was initiated to investigate the cardiac hypertrophic effect of Rosiglitazone in a cellular model of primary neonatal rat cardiomyocytes (NRCM). We assessed whether the drug alters cardiac hypertrophy and its relationship with histone H3 phosphorylation. Our study showed that Rosiglitazone is a mild pro-hypertrophic agent. Rosiglitazone caused a significant increase in the release of brain natriuretic peptide (BNP) into the cell media and also increased cardiomyocytes surface area and atrial natriuretic peptide (ANP) protein expression significantly. These changes correlated with increased cardiac phosphorylation of p38 MAPK and enhanced phosphorylation of H3 at serine 10 globally and at one cardiac hypertrophic gene locus. These results demonstrate that Rosiglitazone causes direct cardiac hypertrophy in NRCM and alters H3 phosphorylation status. They suggest a new mechanism of Rosiglitazone cardiotoxicity implicating chromatin remodeling secondary to H3 phosphorylation, which activate the fetal cardiac gene program.
[Mh] Termos MeSH primário: Cardiomegalia/induzido quimicamente
Montagem e Desmontagem da Cromatina/efeitos dos fármacos
Fibrinolíticos/toxicidade
Miócitos Cardíacos/efeitos dos fármacos
Tiazolidinedionas/toxicidade
[Mh] Termos MeSH secundário: Animais
Fator Natriurético Atrial/metabolismo
Epigênese Genética
Feminino
Fibrinolíticos/administração & dosagem
Regulação da Expressão Gênica/efeitos dos fármacos
Histonas/metabolismo
Miócitos Cardíacos/citologia
Miócitos Cardíacos/metabolismo
Ratos
Ratos Sprague-Dawley
Tiazolidinedionas/administração & dosagem
Proteínas Quinases p38 Ativadas por Mitógeno/genética
Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fibrinolytic Agents); 0 (Histones); 0 (Thiazolidinediones); 05V02F2KDG (rosiglitazone); 85637-73-6 (Atrial Natriuretic Factor); EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170821
[St] Status:MEDLINE


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[PMID]:28635127
[Au] Autor:Rydén M; Arner P
[Ad] Endereço:Department of Medicine (H7), C2-94, Karolinska Institutet at Karolinska University Hospital, Huddinge, Stockholm, Sweden.
[Ti] Título:Cardiovascular risk score is linked to subcutaneous adipocyte size and lipid metabolism.
[So] Source:J Intern Med;282(3):220-228, 2017 Sep.
[Is] ISSN:1365-2796
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Although white adipose tissue mass and distribution correlates with cardiovascular disease, the fat cell-specific perturbations underlying this association are not known. We determined the relationship between adipocyte size and lipid metabolism with cardiovascular risk. DESIGN/SUBJECTS: Adipocyte size as well as spontaneous (basal) and hormone-stimulated effects on adipocyte lipid metabolism (lipolysis and lipogenesis) were investigated in abdominal subcutaneous adipose tissue of 304 men and 775 women. Subjects were classified into five categories according to Adult Treatment Panel III (ATPIII) metabolic syndrome criteria. RESULTS: Adipocyte size increased with increasing ATPIII score (P < 0.0001). For lipolysis, there was a gradual increase in basal and catecholamine-stimulated lipolysis and a decrease in insulin-mediated inhibition of stimulated lipolysis with ATPIII (P < 0.0001). In contrast, the lipolytic action of atrial natriuretic peptide was similar between ATPIII classes. Basal and insulin-stimulated lipogenesis decreased with increasing score (P < 0.0001). Circulating free fatty acid levels were 50% higher in the top risk category (4-5) compared with the lowest score (P < 0.0001). Fat cell size correlated positively with increasing ATPIII score and lipolysis but negatively with lipogenesis. All these differences were independent of age, sex and body weight status (P < 0.0001 to 0.02 after correction). When all functional measures were put together, maximum insulin-stimulated lipogenesis, insulin-antilipolytic sensitivity and basal lipolysis together explained about 20% in the variation of ATPIII in score. CONCLUSIONS: Independently of sex, age and body weight status, a high cardiovascular risk score associates with increased circulating free fatty acid levels and hormone-specific alterations of lipolysis/lipogenesis in enlarged subcutaneous fat cells.
[Mh] Termos MeSH primário: Adipócitos/citologia
Doenças Cardiovasculares/metabolismo
Tamanho Celular
Lipogênese/fisiologia
Lipólise/fisiologia
Medição de Risco
[Mh] Termos MeSH secundário: Adulto
Fatores Etários
Fator Natriurético Atrial/farmacologia
Índice de Massa Corporal
Peso Corporal
Doenças Cardiovasculares/patologia
Ácidos Graxos não Esterificados/sangue
Feminino
Seres Humanos
Insulina/farmacologia
Isoproterenol/farmacologia
Lipogênese/efeitos dos fármacos
Lipólise/efeitos dos fármacos
Masculino
Meia-Idade
Norepinefrina/farmacologia
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fatty Acids, Nonesterified); 0 (Insulin); 85637-73-6 (Atrial Natriuretic Factor); L628TT009W (Isoproterenol); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE
[do] DOI:10.1111/joim.12641


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[PMID]:28596054
[Au] Autor:Nishizawa N; Nakamura G; Noguchi Y; Nakagawa H; Shimizu A; Nakayama M; Takekawa S; Asami T
[Ad] Endereço:Pharmaceutical Research Division, Takeda Pharmaceutical Company Ltd, Fujisawa 251-8555, Japan.
[Ti] Título:A potent and selective natriuretic peptide receptor-3 blocker 11-mer peptide created by hybridization of musclin and atrial natriuretic peptide.
[So] Source:Bioorg Med Chem Lett;27(15):3542-3545, 2017 08 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The natriuretic peptide (NP) system is a critical endocrine, autocrine, and paracrine system and has been investigated for potential use against cardiovascular and metabolic diseases. The clearance of NPs is regulated by the proteolysis of neutral endopeptidase (NEP) and by endocytosis via natriuretic peptide receptor-3 (NPR3). A linear NPR3-selective peptide, [Cha ]-ANP(7-16)-NH (1), showed potent binding affinity for NPR3 but poor predicted chemical stability due to its free thiol group. A 12-mer peptide (9) without a thiol group was designed by the hybridization of two NPR3-binding peptides: a linear ANP fragment peptide analog and musclin, a murine member of the bHLH family of transcription factors, possessed high binding affinity and strict selectivity for NPR3. To increase the proteolytic resistance of 9, amino acid substitutions at the cleavage sites led to hydroxyacetyl-[d-Phe ,d-Hyp ,Cha ,d-Ser ,Hyp ,Arg(Me) ]-ANP(5-15)-NHCH (23), showing high and selective binding affinity for NPR3 over NPR1 and excellent stability in mouse serum. Compound 23 increased intracellular cGMP concentrations in primary cultured adipocytes, and continuous administration induced substantial plasma cGMP elevation in mice, suggesting its potential to clarify the physiological role of NPR3 and its therapeutic application.
[Mh] Termos MeSH primário: Fator Natriurético Atrial/farmacologia
Proteínas Musculares/farmacologia
Fragmentos de Peptídeos/farmacologia
Receptores do Fator Natriurético Atrial/antagonistas & inibidores
Fatores de Transcrição/farmacologia
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Fator Natriurético Atrial/administração & dosagem
Fator Natriurético Atrial/sangue
Fator Natriurético Atrial/química
Camundongos
Camundongos Endogâmicos C57BL
Proteínas Musculares/administração & dosagem
Proteínas Musculares/sangue
Proteínas Musculares/química
Fragmentos de Peptídeos/administração & dosagem
Fragmentos de Peptídeos/sangue
Fragmentos de Peptídeos/química
Receptores do Fator Natriurético Atrial/metabolismo
Fatores de Transcrição/administração & dosagem
Fatores de Transcrição/sangue
Fatores de Transcrição/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Muscle Proteins); 0 (OSTN protein, human); 0 (Peptide Fragments); 0 (Transcription Factors); 85637-73-6 (Atrial Natriuretic Factor); EC 4.6.1.2 (Receptors, Atrial Natriuretic Factor); EC 4.6.1.2 (atrial natriuretic factor receptor C)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171125
[Lr] Data última revisão:
171125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170610
[St] Status:MEDLINE


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[PMID]:28535942
[Au] Autor:Liu X; Zhang Y; Hong L; Han CJ; Zhang B; Zhou S; Wu CZ; Liu LP; Cui X
[Ad] Endereço:Department of Physiology, School of Medical Sciences, Yanbian University, Yanji 133-002, China.
[Ti] Título:Gallic acid increases atrial natriuretic peptide secretion and mechanical dynamics through activation of PKC.
[So] Source:Life Sci;181:45-52, 2017 Jul 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Gallic acid (GA) protects against myocardial ischemia-reperfusion (I/R) injury, prevents cardiac hypertrophy and fibrosis, and has anti-inflammatory activity in the heart. However, its effects in regulating atrial natriuretic peptide (ANP) secretion are unknown. The aim of this study was to determine the function of GA in regulating ANP secretion and atrial dynamics in rat atria. KEY FINDINGS: GA (0.01, 0.05, and 0.1µmol/L) significantly increased atrial ANP secretion and induced positive inotropy dose-dependently. GA (0.1µmol/L) also increased plasma level of ANP and hemodynamics in rats. These effects were accompanied by upregulation of atrial protein kinase C subtypes ß and ε (PKC and PKC ), which was completely blocked by LY333531 and EAVSLKPT, antagonists of protein PKC and PKC , respectively. GA-induced ANP secretion was also attenuated by Gö6983 but not rottlerin, antagonists of PKC and PKC , and the positive inotropy was reversed by Gö6983. U-73122, a phospholipase C (PLC) antagonist, mitigated the effects of GA on ANP secretion and mechanical dynamics and downregulated Phospho-PLC at Ser (pPLC S537), Phospho-PLC at Ser (pPLC S1105), PKC and PKC levels, whereas KN62, an inhibitor of Ca /calmodulin-dependent kinase II, was not modified the GA-induced ANP secretion and suppressed GA-induced mechanical dynamics. SIGNIFICANCE: GA promotes ANP secretion and effects positive inotropy with regard to mechanical dynamics through the activation of PLC-PKC signaling in rat atria.
[Mh] Termos MeSH primário: Fator Natriurético Atrial/efeitos dos fármacos
Ácido Gálico/farmacologia
Átrios do Coração/efeitos dos fármacos
Fosfolipases Tipo C/metabolismo
[Mh] Termos MeSH secundário: Animais
Fator Natriurético Atrial/sangue
Fator Natriurético Atrial/secreção
Relação Dose-Resposta a Droga
Feminino
Ácido Gálico/administração & dosagem
Átrios do Coração/metabolismo
Masculino
Proteína Quinase C beta/metabolismo
Proteína Quinase C-épsilon/metabolismo
Ratos
Ratos Sprague-Dawley
Transdução de Sinais/efeitos dos fármacos
Regulação para Cima/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
632XD903SP (Gallic Acid); 85637-73-6 (Atrial Natriuretic Factor); EC 2.7.11.13 (Protein Kinase C beta); EC 2.7.11.13 (Protein Kinase C-epsilon); EC 3.1.4.- (Type C Phospholipases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170911
[Lr] Data última revisão:
170911
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170525
[St] Status:MEDLINE


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[PMID]:28513772
[Au] Autor:Li Q; Yu Q; Na R; Liu B
[Ad] Endereço:Zhejiang Province Hospital of Integrated Traditional Chinese and Western Medicine, Hangzhou, China.
[Ti] Título:Etanercept protects rat cardiomyocytes against hypertrophy by regulating inflammatory cytokines secretion and cell apoptosis.
[So] Source:Braz J Med Biol Res;50(6):e5868, 2017 May 15.
[Is] ISSN:1414-431X
[Cp] País de publicação:Brazil
[La] Idioma:eng
[Ab] Resumo:We aimed to investigate the effect of etanercept, a tumor necrosis factor-α (TNF-α) inhibitor, on rat cardiomyocyte hypertrophy and its underlying mechanism. Primary neonatal rat cardiomyocytes were isolated from Sprague-Dawley rats. The model of rat cardiomyocyte hypertrophy was induced by endothelin, and then treated with different concentrations of etanercept (1, 10, and 50 µM). After treatment, cell counts, viability and cell apoptosis were evaluated. The mRNA levels of myocardial hypertrophy marker genes, including atrial natriuretic factor (ANF), matrix metalloproteinase (MMP)-9 and MMP-13, were detected by qRT-PCR, and the expressions of apoptosis-related proteins (Bcl-2 and Bax) were measured by western blotting. The protein levels of transforming growth factor-ß1 (TGF-ß1), interleukin (IL)-1ß, IL-6, leukemia inhibitory factor (LIF) and cardiotrophin-1 (CT-1) were determined using enzyme linked immunosorbent assay (ELISA) kits. In the present study, TNF-α level in cardiomyocytes with hypertrophy was significantly enhanced (P<0.05). Compared to the model group, cell number and viability were significantly increased and ratio of apoptotic cells was reduced by etanercept (P<0.05, P<0.01, or P<0.001). In addition, etanercept remarkably reduced the mRNA levels of ANF, MMP-9 and MMP-13, inhibited the expression of Bax, and increased the expression of Bcl-2 compared to the model group (P<0.05). ELISA results further showed that etanercept lowered the levels of IL-1ß, IL-6, LIF and CT-1 but not TGF-ß1 compared to the model group (P<0.05). Etanercept may protect rat cardiomyocytes from hypertrophy by inhibiting inflammatory cytokines secretion and cell apoptosis.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Cardiomegalia/metabolismo
Etanercepte/farmacologia
Miócitos Cardíacos/efeitos dos fármacos
Substâncias Protetoras/farmacologia
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Apoptose/efeitos dos fármacos
Fator Natriurético Atrial/metabolismo
Cardiomegalia/induzido quimicamente
Proliferação Celular/efeitos dos fármacos
Sobrevivência Celular/efeitos dos fármacos
Células Cultivadas
Citocinas/efeitos dos fármacos
Modelos Animais de Doenças
Inflamação/metabolismo
Metaloproteinase 13 da Matriz/metabolismo
Metaloproteinase 9 da Matriz/metabolismo
Miócitos Cardíacos/metabolismo
Ratos Sprague-Dawley
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Cytokines); 0 (Protective Agents); 0 (Tumor Necrosis Factor-alpha); 85637-73-6 (Atrial Natriuretic Factor); EC 3.4.24.- (Matrix Metalloproteinase 13); EC 3.4.24.35 (Matrix Metalloproteinase 9); OP401G7OJC (Etanercept)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170925
[Lr] Data última revisão:
170925
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170518
[St] Status:MEDLINE



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