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  1 / 19310 MEDLINE  
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[PMID]:29428027
[Au] Autor:Allen CJ; Subhawong TK; Hanna MM; Chelala L; Bullock MR; Schulman CI; Proctor KG
[Ti] Título:Does Vasopressin Exacerbate Cerebral Edema in Patients with Severe Traumatic Brain Injury?
[So] Source:Am Surg;84(1):43-50, 2018 Jan 01.
[Is] ISSN:1555-9823
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Arginine vasopressin (AVP) is often used as an alternative pressor to catecholamines (CATs). However, unlike CATs, AVP is a powerful antidiuretic that could promote edema. We tested the hypothesis that AVP promoted cerebral edema and/or increased requirements for osmotherapy, relative to those who received CATs, for cerebral perfusion pressure (CPP) management after traumatic brain injury (TBI). This is a retrospective review of 286 consecutive TBI patients with intracranial pressure monitoring at a single institution from September 2008 to January 2015. Cerebral edema was quantitated using CT attenuation in prespecified areas of gray and white matter. RESULTS: To maintain CPP >60 mm Hg, 205 patients required no vasopressors, 41 received a single CAT, 12 received AVP, and 28 required both. Those who required no pressors were generally less injured; required less hyperosmolar therapy and less total fluid; and had lower plasma Na, lower intracranial pressure, less edema, and lower mortality (all P < 0.05). Edema; daily mean, minimum, and maximum Na levels; and mortality were similar with AVP versus CATs, but the daily requirement of mannitol and 3 per cent NaCl were reduced by 45 and 35 per cent (both P < 0.05). In patients with TBI who required CPP therapy, AVP reduced the requirements for hyperosmolar therapy and did not delay resolution or increase cerebral edema compared with CATs.
[Mh] Termos MeSH primário: Edema Encefálico/tratamento farmacológico
Lesões Encefálicas Traumáticas/tratamento farmacológico
Circulação Cerebrovascular/efeitos dos fármacos
Vasoconstritores/administração & dosagem
Vasopressinas/administração & dosagem
[Mh] Termos MeSH secundário: Adulto
Edema Encefálico/diagnóstico
Edema Encefálico/etiologia
Edema Encefálico/mortalidade
Lesões Encefálicas Traumáticas/complicações
Lesões Encefálicas Traumáticas/diagnóstico
Lesões Encefálicas Traumáticas/mortalidade
Catecolaminas/uso terapêutico
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Retrospectivos
Índices de Gravidade do Trauma
Resultado do Tratamento
Vasoconstritores/efeitos adversos
Vasopressinas/efeitos adversos
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Catecholamines); 0 (Vasoconstrictor Agents); 11000-17-2 (Vasopressins)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180212
[St] Status:MEDLINE


  2 / 19310 MEDLINE  
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[PMID]:29232236
[Au] Autor:Fan JR; Faraday N
[Ad] Endereço:Johns Hopkins University School of Medicine, Baltimore, Maryland (N.F.). nfaraday@jhmi.edu.
[Ti] Título:Vasopressin versus Norepinephrine after Cardiopulmonary Bypass.
[So] Source:Anesthesiology;128(1):229-230, 2018 01.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Ponte Cardiopulmonar
Norepinefrina
[Mh] Termos MeSH secundário: Seres Humanos
Vasopressinas
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T; COMMENT
[Nm] Nome de substância:
11000-17-2 (Vasopressins); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0000000000001956


  3 / 19310 MEDLINE  
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[PMID]:29232235
[Au] Autor:James A; Amour J
[Ad] Endereço:Hôpital Pitié-Salpêtrière, Assistance Publique-Hôpitaux de Paris, Paris, France (A.J.). arthur.a.james@orange.fr.
[Ti] Título:Vasopressin versus Norepinephrine in Patients with Vasoplegic Shock after Cardiac Surgery: A Discussion of the Level of Evidence.
[So] Source:Anesthesiology;128(1):228, 2018 01.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Norepinefrina
Vasopressinas
[Mh] Termos MeSH secundário: Seres Humanos
Choque
Choque Séptico
Vasoconstritores
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
0 (Vasoconstrictor Agents); 11000-17-2 (Vasopressins); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0000000000001955


  4 / 19310 MEDLINE  
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[PMID]:29232234
[Au] Autor:Jha AK
[Ad] Endereço:All India Institute of Medical Sciences, Bhubaneswar, India. drajaykjha@rediffmail.com.
[Ti] Título:Use of Vasopressin in Vasoplegic Syndrome with Reduced Ejection Fraction: Asking for Trouble.
[So] Source:Anesthesiology;128(1):227, 2018 01.
[Is] ISSN:1528-1175
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Volume Sistólico
Vasoplegia
[Mh] Termos MeSH secundário: Seres Humanos
Vasopressinas
[Pt] Tipo de publicação:LETTER; COMMENT
[Nm] Nome de substância:
11000-17-2 (Vasopressins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1097/ALN.0000000000001954


  5 / 19310 MEDLINE  
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[PMID]:29200428
[Au] Autor:Laviola G; Zoratto F; Ingiosi D; Carito V; Huzard D; Fiore M; Macrì S
[Ad] Endereço:Reference Centre for Behavioural Sciences and Mental Health, Istituto Superiore di Sanità (ISS), Rome, Italy.
[Ti] Título:Low empathy-like behaviour in male mice associates with impaired sociability, emotional memory, physiological stress reactivity and variations in neurobiological regulations.
[So] Source:PLoS One;12(12):e0188907, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Deficits in empathy have been proposed to constitute a hallmark of several psychiatric disturbances like conduct disorder, antisocial and narcissistic personality disorders. Limited sensitivity to punishment, shallow or deficient affect and reduced physiological reactivity to environmental stressors have been often reported to co-occur with limited empathy and contribute to the onset of antisocial phenotypes. Empathy in its simplest form (i.e. emotional contagion) is addressed in preclinical models through the evaluation of the social transmission of emotional states: mice exposed to a painful stimulus display a higher response if in the presence of a familiar individual experiencing a higher degree of discomfort, than in isolation. In the present study, we investigated whether a reduction of emotional contagion can be considered a predictor of reduced sociality, sensitivity to punishment and physiological stress reactivity. To this aim, we first evaluated emotional contagion in a group of Balb/cJ mice and then discretised their values in four quartiles. The upper (i.e. Emotional Contagion Prone, ECP) and the lower (i.e. Emotional Contagion Resistant, ECR) quartiles constituted the experimental groups. Our results indicate that mice in the lower quartile are characterized by reduced sociability, impaired memory of negative events and dampened hypothalamic-pituitary-adrenocortical reactivity to external stressors. Furthermore, in the absence of changes in oxytocin receptor density, we show that these mice exhibit elevated concentrations of oxytocin and vasopressin and reduced density of BDNF receptors in behaviourally-relevant brain areas. Thus, not only do present results translate to the preclinical investigation of psychiatric disturbances, but also they can contribute to the study of emotional contagion in terms of its adaptive significance.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Emoções/fisiologia
Empatia/fisiologia
Memória/fisiologia
Estresse Fisiológico/fisiologia
[Mh] Termos MeSH secundário: Animais
Sistema Hipotálamo-Hipofisário/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Ocitocina/metabolismo
Receptor trkB/metabolismo
Receptores de Ocitocina/metabolismo
Vasopressinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Oxytocin); 11000-17-2 (Vasopressins); 50-56-6 (Oxytocin); EC 2.7.10.1 (Receptor, trkB)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171229
[Lr] Data última revisão:
171229
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188907


  6 / 19310 MEDLINE  
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[PMID]:28974518
[Au] Autor:Yang G; Peng X; Wu Y; Li T; Liu L
[Ad] Endereço:State Key Laboratory of Trauma, Burns, and Combined Injury, Second Department of Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing, China.
[Ti] Título:Involvement of connexin 43 phosphorylation and gap junctional communication between smooth muscle cells in vasopressin-induced ROCK-dependent vasoconstriction after hemorrhagic shock.
[So] Source:Am J Physiol Cell Physiol;313(4):C362-C370, 2017 Oct 01.
[Is] ISSN:1522-1563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We examined the roles played by gap junctions (GJs) and the GJ channel protein connexin 43 (Cx43) in arginine vasopressin (AVP)-induced vasoconstriction after hemorrhagic shock and their relationship to Rho kinase (ROCK) and protein kinase C (PKC). The results showed that AVP induced an endothelium-independent contraction in rat superior mesenteric arteries (SMAs). Blocking the GJs significantly decreased the contractile response of SMAs and vascular smooth muscle cells (VSMCs) to AVP after shock and hypoxia. The selective Cx43-mimetic peptide inhibited the vascular contractile effect of AVP after shock and hypoxia. AVP restored hypoxia-induced decrease of Cx43 phosphorylation at Ser and gap junctional communication in VSMCs. Activation of RhoA with U-46619 increased the contractile effect of AVP. This effect was antagonized by the ROCK inhibitor Y27632 and the Cx43-mimetic peptide. In contrast, neither an agonist nor an inhibitor of PKC had significant effects on AVP-induced contraction after hemorrhagic shock. In addition, silencing of Cx43 with siRNA blocked the AVP-induced increase of ROCK activity in hypoxic VSMCs. In conclusion, AVP-mediated vascular contractile effects are endothelium and myoendothelial gap junction independent. Gap junctions between VSMCs, gap junctional communication, and Cx43 phosphorylation at Ser play important roles in the vascular effects of AVP. RhoA/ROCK, but not PKC, is involved in this process.
[Mh] Termos MeSH primário: Junções Comunicantes/metabolismo
Miócitos de Músculo Liso/metabolismo
Choque Hemorrágico/tratamento farmacológico
Choque Hemorrágico/metabolismo
Vasoconstrição/efeitos dos fármacos
Vasopressinas/administração & dosagem
Quinases Associadas a rho/metabolismo
[Mh] Termos MeSH secundário: Animais
Conexina 43
Ativação Enzimática/efeitos dos fármacos
Feminino
Junções Comunicantes/efeitos dos fármacos
Masculino
Miócitos de Músculo Liso/efeitos dos fármacos
Ratos Sprague-Dawley
Resultado do Tratamento
Vasoconstritores/administração & dosagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Connexin 43); 0 (Vasoconstrictor Agents); 0 (connexin 43 protein, rat); 11000-17-2 (Vasopressins); EC 2.7.11.1 (rho-Associated Kinases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171005
[St] Status:MEDLINE
[do] DOI:10.1152/ajpcell.00258.2016


  7 / 19310 MEDLINE  
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[PMID]:28920920
[Au] Autor:Shi G; Somlo DRM; Kim GH; Prescianotto-Baschong C; Sun S; Beuret N; Long Q; Rutishauser J; Arvan P; Spiess M; Qi L
[Ad] Endereço:Department of Molecular and Integrative Physiology, University of Michigan Medical School, Ann Arbor, Michigan, USA.
[Ti] Título:ER-associated degradation is required for vasopressin prohormone processing and systemic water homeostasis.
[So] Source:J Clin Invest;127(10):3897-3912, 2017 10 02.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peptide hormones are crucial regulators of many aspects of human physiology. Mutations that alter these signaling peptides are associated with physiological imbalances that underlie diseases. However, the conformational maturation of peptide hormone precursors (prohormones) in the ER remains largely unexplored. Here, we report that conformational maturation of proAVP, the precursor for the antidiuretic hormone arginine-vasopressin, within the ER requires the ER-associated degradation (ERAD) activity of the Sel1L-Hrd1 protein complex. Serum hyperosmolality induces expression of both ERAD components and proAVP in AVP-producing neurons. Mice with global or AVP neuron-specific ablation of Se1L-Hrd1 ERAD progressively developed polyuria and polydipsia, characteristics of diabetes insipidus. Mechanistically, we found that ERAD deficiency causes marked ER retention and aggregation of a large proportion of all proAVP protein. Further, we show that proAVP is an endogenous substrate of Sel1L-Hrd1 ERAD. The inability to clear misfolded proAVP with highly reactive cysteine thiols in the absence of Sel1L-Hrd1 ERAD causes proAVP to accumulate and participate in inappropriate intermolecular disulfide-bonded aggregates, promoted by the enzymatic activity of protein disulfide isomerase (PDI). This study highlights a pathway linking ERAD to prohormone conformational maturation in neuroendocrine cells, expanding the role of ERAD in providing a conducive ER environment for nascent proteins to reach proper conformation.
[Mh] Termos MeSH primário: Degradação Associada com o Retículo Endoplasmático
Retículo Endoplasmático/metabolismo
Células Neuroendócrinas/metabolismo
Proteólise
Vasopressinas/metabolismo
Equilíbrio Hidroeletrolítico
[Mh] Termos MeSH secundário: Animais
Retículo Endoplasmático/genética
Camundongos
Camundongos Transgênicos
Células Neuroendócrinas/patologia
Neurônios/metabolismo
Neurônios/patologia
Polidipsia/genética
Polidipsia/metabolismo
Polidipsia/patologia
Isomerases de Dissulfetos de Proteínas/genética
Isomerases de Dissulfetos de Proteínas/metabolismo
Proteínas/genética
Proteínas/metabolismo
Ubiquitina-Proteína Ligases/genética
Ubiquitina-Proteína Ligases/metabolismo
Vasopressinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Proteins); 0 (Sel1h protein, mouse); 0 (proAVP hormone); 11000-17-2 (Vasopressins); EC 2.3.2.27 (Syvn1 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 5.3.4.1 (Protein Disulfide-Isomerases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171114
[Lr] Data última revisão:
171114
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170919
[St] Status:MEDLINE


  8 / 19310 MEDLINE  
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[PMID]:28905441
[Au] Autor:Clark WF; Devuyst O; Roussel R
[Ad] Endereço:Division of Nephrology, Department of Medicine, London Health Sciences Centre, London, ON, Canada.
[Ti] Título:The vasopressin system: new insights for patients with kidney diseases: Epidemiological evidence and therapeutic perspectives.
[So] Source:J Intern Med;282(4):310-321, 2017 Oct.
[Is] ISSN:1365-2796
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:People with chronic kidney disease (CKD) are at risk of severe outcomes, such as end-stage renal disease or cardiovascular disease, and CKD is a globally increasing health burden with a high personal and economic cost. Despite major progresses in prevention and therapeutics in last decades, research is still needed to reverse this epidemic trend. The regulation of water balance and the state of activation of the vasopressin system have emerged as factors tightly associated with kidney health, in the general population but also in specific conditions; among them, various stages of CKD, diabetes and autosomal dominant polycystic kidney disease (ADPKD). Basic science findings and also epidemiological evidence have justified important efforts towards interventional studies supporting causality, and opening therapeutic avenues. On the basis of recent clinical data, the blockade of V2 vasopressin receptors using tolvaptan in patients with rapidly progressing ADPKD has been granted in several countries, and a long-term randomized trial evaluating the effect of an increase in water intake in patients with CKD is on-going.
[Mh] Termos MeSH primário: Nefropatias/fisiopatologia
Vasopressinas/fisiologia
[Mh] Termos MeSH secundário: Antagonistas de Receptores de Hormônios Antidiuréticos/uso terapêutico
Biomarcadores/sangue
Nefropatias Diabéticas/sangue
Nefropatias Diabéticas/fisiopatologia
Hidratação
Glicopeptídeos/sangue
Glicopeptídeos/fisiologia
Seres Humanos
Rim/fisiopatologia
Nefropatias/epidemiologia
Nefropatias/terapia
Rim Policístico Autossômico Dominante/tratamento farmacológico
Insuficiência Renal Crônica/epidemiologia
Insuficiência Renal Crônica/fisiopatologia
Insuficiência Renal Crônica/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antidiuretic Hormone Receptor Antagonists); 0 (Biomarkers); 0 (Glycopeptides); 0 (copeptins); 11000-17-2 (Vasopressins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1111/joim.12654


  9 / 19310 MEDLINE  
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[PMID]:28754320
[Au] Autor:Zhang Q; Liu B; Zhao L; Qi Z; Shao H; An L; Li C
[Ad] Endereço:Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing Chao-Yang Hospital,Capital Medical University, Beijing 100020, China.
[Ti] Título:Efficacy of vasopressin-epinephrine compared to epinephrine alone for out of hospital cardiac arrest patients: A systematic review and meta-analysis.
[So] Source:Am J Emerg Med;35(10):1555-1560, 2017 Oct.
[Is] ISSN:1532-8171
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The aim of this study was to conduct a meta-analysis to evaluate the efficacy of vasopressin-epinephrine compared to epinephrine alone in patients who suffered out-of-hospital cardiac arrest (OHCA). METHODS: Relevant studies up to February 2017 were identified by searching in PubMed, EMBASE, the Cochrane Library, Wanfang for randomized controlled trials(RCTs) assigning adults with cardiac arrest to treatment with vasopressin-epinephrine (VEgroup) vs adrenaline (epinephrine) alone (E group). The outcome point was return of spontaneous circulation (ROSC) for patients suffering from OHCA. Heterogeneity, subgroup analysis, sensitivity analysis and publication bias were explored. RESULTS: Individual patient data were obtained from 5047 participants who experienced OHCA in nine studies. Odds ratios (ORs) were calculated using a random-effects model and results suggested that vasopressin-epinephrine was associated with higher rate of ROSC (OR=1.67, 95% CI=1.13-2.49, P<0.00001, and total I =83%). Subgroup showed that vasopressin-epinephrine has a significant association with improvements in ROSC for patients from Asia (OR=3.30, 95% CI=1.30-7.88); but for patients from other regions, there was no difference between vasopressin-epinephrine and epinephrine alone (OR=1.07, 95% CI=0.72-1.61). CONCLUSION: According to the pooled results of the subgroup, combination of vasopressin and adrenaline can improve ROSC of OHCA from Asia, but patients from other regions who suffered from OHCA cannot benefit from combination of vasopressin and epinephrine.
[Mh] Termos MeSH primário: Reanimação Cardiopulmonar/métodos
Epinefrina/uso terapêutico
Parada Cardíaca Extra-Hospitalar/terapia
Vasopressinas/uso terapêutico
[Mh] Termos MeSH secundário: Quimioterapia Combinada
Seres Humanos
Resultado do Tratamento
Vasoconstritores/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; REVIEW
[Nm] Nome de substância:
0 (Vasoconstrictor Agents); 11000-17-2 (Vasopressins); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170730
[St] Status:MEDLINE


  10 / 19310 MEDLINE  
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[PMID]:28714397
[Au] Autor:Golembiewska E; Machowska A; Stenvinkel P; Lindholm B
[Ad] Endereço:Department of Nephrology, Transplantology and Internal Medicine, Pomeranian Medical University, Al. Powstancow Wielkopolskich 72, 70-111 Szczecin. Poland.
[Ti] Título:Prognostic Value of Copeptin in Chronic Kidney Disease: From General Population to End-Stage Renal Disease.
[So] Source:Curr Protein Pept Sci;18(12):1232-1243, 2017.
[Is] ISSN:1875-5550
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Arginine vasopressin (AVP), also known as antidiuretic hormone (ADH), is released in response to osmotic and non-osmotic stimuli and plays a key role in many physiologic and pathologic processes. The main function of AVP is the control of fluid homeostasis by inducing water conservation by the kidney, but it also stimulates arteriolar vasoconstriction and the release of adrenocorticotropic hormone (ACTH). These actions are mediated by different AVP receptors located on various target cells. Produced in hypothalamus from a larger precursor, pre-proAVP, AVP is produced in equimolar amounts to copeptin, a glycopeptide with yet unknown biologic function. Copeptin remains stable in plasma and its circulating concentrations correlate directly with those of AVP. Because AVP is unstable in isolated plasma or serum and its half-life is short, copeptin has become an easily measured surrogate marker reflecting vasopressin concentration. Recently, associations between high circulating copeptin and decline in glomerular filtration rate as well as greater risk of new-onset chronic kidney disease (CKD) have been reported. In addition, copeptin has been shown to be associated with increased risk of complications such as myocardial infarction, heart failure, diabetes mellitus and metabolic syndrome. In this brief review, studies on the prognostic value of copeptin measurement in the general population and in CKD are presented and discussed.
[Mh] Termos MeSH primário: Arginina Vasopressina/genética
Glicopeptídeos/genética
Hipotálamo/metabolismo
Falência Renal Crônica/diagnóstico
[Mh] Termos MeSH secundário: Hormônio Adrenocorticotrópico/sangue
Hormônio Adrenocorticotrópico/genética
Arginina Vasopressina/sangue
Biomarcadores/sangue
Progressão da Doença
Feminino
Regulação da Expressão Gênica
Taxa de Filtração Glomerular
Glicopeptídeos/sangue
Seres Humanos
Falência Renal Crônica/sangue
Falência Renal Crônica/genética
Falência Renal Crônica/patologia
Masculino
Prognóstico
Receptores de Vasopressinas/sangue
Receptores de Vasopressinas/genética
Fatores Sexuais
Transdução de Sinais
Vasopressinas/sangue
Vasopressinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Biomarkers); 0 (Glycopeptides); 0 (Receptors, Vasopressin); 0 (copeptins); 0 (proAVP hormone); 11000-17-2 (Vasopressins); 113-79-1 (Arginine Vasopressin); 9002-60-2 (Adrenocorticotropic Hormone)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170718
[St] Status:MEDLINE
[do] DOI:10.2174/1389203718666170717095301



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