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[PMID]:28217833
[Au] Autor:Spasic M; Jacobs CR
[Ti] Título:Lengthening primary cilia enhances cellular mechanosensitivity.
[So] Source:Eur Cell Mater;33:158-168, 2017 Feb 20.
[Is] ISSN:1473-2262
[Cp] País de publicação:Scotland
[La] Idioma:eng
[Ab] Resumo:The primary cilium is a mechanosensor in a variety of mammalian cell types, initiating and directing intracellular signalling cascades in response to external stimuli. When primary cilia formation is disrupted, cells have diminished mechanosensitivity and an abrogated response to mechanical stimulation. Due to this important role, we hypothesised that increasing primary cilia length would enhance the downstream response and therefore, mechanosensitivity. To test this hypothesis, we increased osteocyte primary cilia length with fenoldopam and lithium and found that cells with longer primary cilia were more mechanosensitive. Furthermore, fenoldopam treatment potentiated adenylyl cyclase activity and was able to recover primary cilia form and sensitivity in cells with impaired cilia. This work demonstrates that modulating the structure of the primary cilium directly impacts cellular mechanosensitivity. Our results implicate cilium length as a potential therapeutic target for combating numerous conditions characterised by impaired cilia function.
[Mh] Termos MeSH primário: Cílios/metabolismo
Mecanotransdução Celular
[Mh] Termos MeSH secundário: Adenilil Ciclases/metabolismo
Animais
Linhagem Celular
Cílios/efeitos dos fármacos
Fenoldopam/farmacologia
Mecanotransdução Celular/efeitos dos fármacos
Camundongos
RNA Interferente Pequeno/metabolismo
Bibliotecas de Moléculas Pequenas/farmacologia
Proteínas Supressoras de Tumor/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (Small Molecule Libraries); 0 (Tg737Rpw protein, mouse); 0 (Tumor Suppressor Proteins); EC 4.6.1.1 (Adenylyl Cyclases); INU8H2KAWG (Fenoldopam)
[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:170221
[St] Status:MEDLINE
[do] DOI:10.22203/eCM.v033a12


  2 / 603 MEDLINE  
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[PMID]:27996211
[Au] Autor:Wang JR; Sun PH; Ren ZX; Meltzer HY; Zhen XC
[Ad] Endereço:Jiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Soochow University, Suzhou, Jiangsu, China.
[Ti] Título:GSK-3ß Interacts with Dopamine D1 Receptor to Regulate Receptor Function: Implication for Prefrontal Cortical D1 Receptor Dysfunction in Schizophrenia.
[So] Source:CNS Neurosci Ther;23(2):174-187, 2017 Feb.
[Is] ISSN:1755-5949
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Impaired dopamine D1 receptor (D1R) function in prefrontal cortex (PFC) is believed to contribute to the PFC hypofunction that has been hypothesized to be associated with negative symptoms and cognitive deficits in schizophrenia. It is therefore critical to understand the mechanisms for modulation of D1R function. AIMS: To investigate the physical interaction and functional modulation between D1R and GSK-3ß. RESULTS: D1R and GSK-3ß physically interact in cultured cells and native brain tissues. This direct interaction was found to occur at the S(417)PALS(421) motif in the C-terminus of D1R. Inhibition of GSK-3ß impaired D1R activation along with a decrease in D1R-GSK-3ß interaction. GSK-3ß inhibition reduced agonist-stimulated D1R desensitization and endocytosis, the latter associated with the reduction of membrane translocation of ß-arrestin-2. Similarly, inhibition of GSK-3ß in rat PFC also resulted in impaired D1R activation and association with GSK-3ß. Moreover, in a NMDA antagonist animal model of schizophrenia, we detected a decrease in prefrontal GSK-3ß activity and D1R-GSK-3ß association and decreased D1R activation in the PFC. CONCLUSIONS: The present work identified GSK-3ß as a new interacting protein for D1R functional regulation and revealed a novel mechanism for GSK-3ß-regulated D1R function which may underlie D1R dysfunction in schizophrenia.
[Mh] Termos MeSH primário: Glicogênio Sintase Quinase 3 beta/metabolismo
Córtex Pré-Frontal/metabolismo
Receptores de Dopamina D1/metabolismo
Esquizofrenia/metabolismo
Esquizofrenia/patologia
[Mh] Termos MeSH secundário: Adjuvantes Imunológicos/farmacologia
Animais
AMP Cíclico/metabolismo
Modelos Animais de Doenças
Agonistas de Dopamina/farmacologia
Endocitose/efeitos dos fármacos
Endocitose/genética
Inibidores Enzimáticos/farmacologia
Fenoldopam/farmacologia
Glicogênio Sintase Quinase 3 beta/genética
Guanosina 5'-O-(3-Tiotrifosfato)/farmacocinética
Células HEK293
Seres Humanos
Indóis/farmacologia
Cloreto de Lítio/farmacologia
Maleimidas/farmacologia
Córtex Pré-Frontal/efeitos dos fármacos
Transporte Proteico/efeitos dos fármacos
Ratos
Esquizofrenia/induzido quimicamente
beta-Arrestinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Dopamine Agonists); 0 (Enzyme Inhibitors); 0 (Indoles); 0 (Maleimides); 0 (Receptors, Dopamine D1); 0 (SB 216763); 0 (beta-Arrestins); 37589-80-3 (Guanosine 5'-O-(3-Thiotriphosphate)); E0399OZS9N (Cyclic AMP); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); G4962QA067 (Lithium Chloride); INU8H2KAWG (Fenoldopam)
[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:161221
[St] Status:MEDLINE
[do] DOI:10.1111/cns.12664


  3 / 603 MEDLINE  
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[PMID]:27733575
[Au] Autor:Bone NB; Liu Z; Pittet JF; Zmijewski JW
[Ad] Endereço:Department of Medicine, University of Alabama, Birmingham, Alabama, USA; and.
[Ti] Título:Frontline Science: D1 dopaminergic receptor signaling activates the AMPK-bioenergetic pathway in macrophages and alveolar epithelial cells and reduces endotoxin-induced ALI.
[So] Source:J Leukoc Biol;101(2):357-365, 2017 Feb.
[Is] ISSN:1938-3673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Catecholamines, including ß-adrenergic and dopaminergic neurotransmitters, have an essential role in regulating the "fight or flight" reflex and also affects immune cell proinflammatory action. However, little is known about whether catecholamines prevent dysfunction of metabolic pathways associated with inflammatory organ injury, including development of acute lung injury (ALI). We hypothesize that selected catecholamines may reduce metabolic alterations in LPS-stimulated macrophages and in the lungs of mice subjected to endotoxin-induced ALI, a situation characterized by diminished activity of AMP-activated protein kinase (AMPK). We found that activation of the dopamine 1 receptor (D1R) with fenoldopam, but not stimulation of adrenergic receptors with norepinephrine, resulted in a robust activation of AMPK in peritoneal macrophages, human monocytes, or alveolar epithelial cells (AECs). Such AMPK activation was mediated by a phospholipase C (PLC)-dependent mechanism. Unlike norepinephrine, D1R activation also prevented Thr172-AMPK dephosphorylation and kinase inactivation in LPS-treated macrophages. Furthermore, we show that a culture of AECs with either fenoldopam or the AMPK activator metformin effectively diminished IL-1ß-induced release of adverse paracrine signaling, which promotes the macrophage proinflammatory response. In vivo, fenoldopam reduced the severity of LPS-induced ALI, including development of pulmonary edema, lung permeability, and production of inflammatory cytokines TNF-α, MIP-2, or KC and HMGB1. Fenoldopam also prevented AMPK dephosphorylation in the lungs of LPS-treated mice and prevented loss of mitochondrial complexes NDUFB8 (complex I) and ATP synthase (complex V). Collectively, these results suggest that dopamine is coupled to AMPK activation, which provides a substantial anti-inflammatory and bioenergetic advantage and reduces the severity of endotoxin-induced ALI.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Lesão Pulmonar Aguda/metabolismo
Células Epiteliais Alveolares/metabolismo
Metabolismo Energético
Macrófagos/metabolismo
Receptores de Dopamina D1/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Lesão Pulmonar Aguda/patologia
Células Epiteliais Alveolares/efeitos dos fármacos
Animais
Citocinas/biossíntese
Transporte de Elétrons/efeitos dos fármacos
Endotoxinas
Ativação Enzimática/efeitos dos fármacos
Fenoldopam/farmacologia
Seres Humanos
Inflamação/patologia
Lipopolissacarídeos
Pulmão/efeitos dos fármacos
Pulmão/metabolismo
Pulmão/patologia
Macrófagos/efeitos dos fármacos
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Modelos Biológicos
Comunicação Parácrina/efeitos dos fármacos
Fosforilação/efeitos dos fármacos
Receptores Adrenérgicos/metabolismo
Índice de Gravidade de Doença
Transdução de Sinais/efeitos dos fármacos
Fosfolipases Tipo C/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytokines); 0 (Endotoxins); 0 (Lipopolysaccharides); 0 (Receptors, Adrenergic); 0 (Receptors, Dopamine D1); EC 2.7.11.31 (AMP-Activated Protein Kinases); EC 3.1.4.- (Type C Phospholipases); INU8H2KAWG (Fenoldopam)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161014
[St] Status:MEDLINE
[do] DOI:10.1189/jlb.3HI0216-068RR


  4 / 603 MEDLINE  
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[PMID]:26824460
[Au] Autor:Yao Y; Yang D; Han Y; Wang W; Wang N; Yang J; Zeng C
[Ad] Endereço:Department of Cardiology, Daping Hospital, Third Military Medical University, Chongqing, P. R. China.
[Ti] Título:Dopamine D1-Like Receptors Suppress the Proliferation of Macrophages Induced by Ox-LDL.
[So] Source:Cell Physiol Biochem;38(1):415-26, 2016.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Oxidized low-density lipoprotein (Ox-LDL) induces macrophage proliferation, a key physiological process which leads to atherosclerosis. The aim of this study was to determine the effects of dopamine D1-like receptors on macrophage proliferation induced by Ox-LDL. METHODS: The expression of dopamine D1-like receptors was determined by immunohistochemistry, reverse transcriptase-polymerase chain reaction (RT-PCR) and immunoblotting. The effect of D1-like receptors on macrophage proliferation induced by Ox-LDL was measured by 3[H]-thymidine incorporation and cell number count. RESULTS: Dopamine D1-like receptors were present in macrophages as determined by immunohistochemistry, RT-PCR and immunoblotting. A D1-like receptor agonist, fenoldopam, which by itself had no effect on macrophage proliferation, inhibited the stimulatory effect of Ox-LDL on macrophage proliferation. This was further confirmed by the D1-like receptor antagonist SCH 23390 blocking the effect of fenoldopam, thereby indicating that the fenoldopam action was receptor specific. Phosphatidylinositol 3-kinase (PI3K/Akt) and mitogen-activated protein kinase (MAPK/ERK) pathways were also involved in the proliferative effect of Ox-LDL because in the presence of PI3K/Akt or MAPK/ERK inhibitors, LY294002 or PD98059, the stimulatory effects of Ox-LDL were blocked. Moreover, the stimulatory effect of Ox-LDL on the phosphorylation of ERK and Akt was significantly reduced by fenoldopam in macrophages. Additional experiments found that both D1 and D5 receptor expression was lower in the peritoneal macrophages from Apolipoprotein E-deficient mice compared to the control C57Bl/6J mice. CONCLUSIONS: Macrophages express D1-like receptors. The activation of the D1-like receptors significantly inhibits Ox-LDL-induced macrophage proliferation, possibly through the inhibition of the PI3K/Akt and MAPK/ERK signaling pathways.
[Mh] Termos MeSH primário: Proliferação Celular/efeitos dos fármacos
Lipoproteínas LDL/toxicidade
Receptores de Dopamina D1/metabolismo
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas E/deficiência
Apolipoproteínas E/genética
Benzazepinas/farmacologia
Células Cultivadas
Fenoldopam/farmacologia
Macrófagos/citologia
Macrófagos/efeitos dos fármacos
Macrófagos/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteína Quinase 1 Ativada por Mitógeno/antagonistas & inibidores
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/antagonistas & inibidores
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Proteínas Quinases Ativadas por Mitógeno/antagonistas & inibidores
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Fosfatidilinositol 3-Quinases/antagonistas & inibidores
Fosfatidilinositol 3-Quinases/metabolismo
Fosforilação/efeitos dos fármacos
Inibidores de Proteínas Quinases/farmacologia
Proteínas Proto-Oncogênicas c-akt/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-akt/metabolismo
Receptores de Dopamina D1/agonistas
Receptores de Dopamina D1/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Benzazepines); 0 (Lipoproteins, LDL); 0 (Protein Kinase Inhibitors); 0 (Receptors, Dopamine D1); 0 (SCH 23390); 0 (oxidized low density lipoprotein); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); INU8H2KAWG (Fenoldopam)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160130
[St] Status:MEDLINE
[do] DOI:10.1159/000438640


  5 / 603 MEDLINE  
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[PMID]:26763106
[Au] Autor:O'Neill KE; Labato MA; Court MH
[Ad] Endereço:St. Francis Veterinary Specialists, Decatur, GA, USA.
[Ti] Título:The pharmacokinetics of intravenous fenoldopam in healthy, awake cats.
[So] Source:J Vet Pharmacol Ther;39(2):202-4, 2016 Apr.
[Is] ISSN:1365-2885
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Fenoldopam is a selective dopamine-1 receptor agonist that improves diuresis by increasing renal blood flow and perfusion and causing peripheral vasodilation. Fenoldopam has been shown to induce diuresis and be well-tolerated in healthy cats. It is used clinically in cats with oliguric kidney injury at doses extrapolated from human medicine and canine studies. The pharmacokinetics in healthy beagle dogs has been reported; however, pharmacokinetic data in cats are lacking. The goal of this study was to determine pharmacokinetic data for healthy, awake cats receiving an infusion of fenoldopam. Six healthy, awake, client-owned cats aged 2-6 years old received a 120-min constant rate infusion of fenoldopam at 0.8 µg/kg/min followed by a 20-min washout period. Ascorbate stabilized plasma samples were collected during and after the infusion for the measurement of fenoldopam concentration by HPLC with mass spectrometry detection. This study showed that the geometric mean of the volume of distribution, clearance, and half-life (198 mL/kg, 46 mL/kg/min, and 3.0 mins) is similar to pharmacokinetic parameters for humans. No adverse events were noted. Fenoldopam at a constant rate infusion of 0.8 µg/kg per min was well tolerated in healthy cats. Based on the results, further evaluation of fenoldopam in cats with kidney disease is recommended.
[Mh] Termos MeSH primário: Gatos/sangue
Agonistas de Dopamina/farmacocinética
Fenoldopam/farmacocinética
[Mh] Termos MeSH secundário: Animais
Agonistas de Dopamina/administração & dosagem
Agonistas de Dopamina/sangue
Feminino
Fenoldopam/administração & dosagem
Fenoldopam/sangue
Meia-Vida
Injeções Intravenosas
Masculino
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dopamine Agonists); INU8H2KAWG (Fenoldopam)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160115
[St] Status:MEDLINE
[do] DOI:10.1111/jvp.12274


  6 / 603 MEDLINE  
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[PMID]:26751218
[Au] Autor:Jiang X; Chen W; Liu X; Wang Z; Liu Y; Felder RA; Gildea JJ; Jose PA; Qin C; Yang Z
[Ad] Endereço:Institute of Laboratory Animal Science, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Centre, Peking Union Medical Collage (PUMC), Beijing, P. R. China.
[Ti] Título:The Synergistic Roles of Cholecystokinin B and Dopamine D5 Receptors on the Regulation of Renal Sodium Excretion.
[So] Source:PLoS One;11(1):e0146641, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Renal dopamine D1-like receptors (D1R and D5R) and the gastrin receptor (CCKBR) are involved in the maintenance of sodium homeostasis. The D1R has been found to interact synergistically with CCKBR in renal proximal tubule (RPT) cells to promote natriuresis and diuresis. D5R, which has a higher affinity for dopamine than D1R, has some constitutive activity. Hence, we sought to investigate the interaction between D5R and CCKBR in the regulation of renal sodium excretion. In present study, we found D5R and CCKBR increase each other's expression in a concentration- and time-dependent manner in the HK-2 cell, the specificity of which was verified in HEK293 cells heterologously expressing both human D5R and CCKBR and in RPT cells from a male normotensive human. The specificity of D5R in the D5R and CCKBR interaction was verified further using a selective D5R antagonist, LE-PM436. Also, D5R and CCKBR colocalize and co-immunoprecipitate in BALB/c mouse RPTs and human RPT cells. CCKBR protein expression in plasma membrane-enriched fractions of renal cortex (PMFs) is greater in D5R-/- mice than D5R+/+ littermates and D5R protein expression in PMFs is also greater in CCKBR-/- mice than CCKBR+/+ littermates. High salt diet, relative to normal salt diet, increased the expression of CCKBR and D5R proteins in PMFs. Disruption of CCKBR in mice caused hypertension and decreased sodium excretion. The natriuresis in salt-loaded BALB/c mice was decreased by YF476, a CCKBR antagonist and Sch23390, a D1R/D5R antagonist. Furthermore, the natriuresis caused by gastrin was blocked by Sch23390 while the natriuresis caused by fenoldopam, a D1R/D5R agonist, was blocked by YF476. Taken together, our findings indicate that CCKBR and D5R synergistically interact in the kidney, which may contribute to the maintenance of normal sodium balance following an increase in sodium intake.
[Mh] Termos MeSH primário: Rim/metabolismo
Natriurese
Receptor de Colecistocinina B/metabolismo
Receptores de Dopamina D5/metabolismo
Sódio/metabolismo
[Mh] Termos MeSH secundário: Animais
Benzazepinas/química
Pressão Sanguínea
Colecistocinina/metabolismo
Feminino
Fenoldopam/química
Gastrinas/química
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Túbulos Renais/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Transgênicos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Benzazepines); 0 (Gastrins); 0 (Receptor, Cholecystokinin B); 0 (SCH 23390); 137750-35-7 (Receptors, Dopamine D5); 9011-97-6 (Cholecystokinin); 9NEZ333N27 (Sodium); INU8H2KAWG (Fenoldopam)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160112
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0146641


  7 / 603 MEDLINE  
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[PMID]:26506071
[Au] Autor:Post EH; Su F; Taccone FS; Hosokawa K; Herpain A; Creteur J; Vincent JL; De Backer D
[Ad] Endereço:Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium.
[Ti] Título:THE EFFECTS OF FENOLDOPAM ON RENAL FUNCTION AND METABOLISM IN AN OVINE MODEL OF SEPTIC SHOCK.
[So] Source:Shock;45(4):385-92, 2016 Apr.
[Is] ISSN:1540-0514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The importance of renal perfusion and metabolism in septic acute kidney injury (AKI) remains unclear. Prophylactic administration of the dopaminergic agent, fenoldopam, has been suggested to reduce the occurrence of AKI, but its effects in septic shock are poorly defined. METHODS: Sepsis was induced in 15 adult female sheep by injecting autologous feces into the abdominal cavity. Two hours later, the animals were randomized to one of three groups: low-dose fenoldopam (1.0 µg/kg/min, n = 5), high-dose fenoldopam (5.0 µg/kg/min, n = 5), or placebo (control, n = 5). A perivascular flow probe was placed around the renal artery and a catheter in the renal vein for measurement of renal blood flow index (RBFI) and oxygen consumption (VO2renI). Metabolism in the renal cortex was evaluated using microdialysis. Serum creatinine was measured 6-hourly and the sublingual microcirculation assessed using sidestream dark-field videomicroscopy. RESULTS: High-dose fenoldopam was associated with a lower RBFI at 18 h (P = 0.032) than in the control group, but VO2renI was maintained by a higher oxygen extraction (P < 0.05 vs. baseline). Sublingual microcirculatory alterations at 18 h were more severe in the high-dose than in the control and low-dose groups (P = 0.021 and P = 0.032). Renal cortex lactate and pyruvate levels increased earlier in the high-dose group than in the other two groups (P < 0.001 vs. baseline). Fenoldopam did not affect creatinine clearance or urine output. CONCLUSIONS: In this model of septic shock, fenoldopam did not improve renal blood flow, worsened microcirculatory alterations, and induced metabolic changes that were indicative of increased glycolysis.
[Mh] Termos MeSH primário: Fenoldopam/farmacologia
Rim
Choque Séptico
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Feminino
Seres Humanos
Rim/metabolismo
Rim/fisiopatologia
Testes de Função Renal
Ovinos
Choque Séptico/tratamento farmacológico
Choque Séptico/metabolismo
Choque Séptico/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
INU8H2KAWG (Fenoldopam)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151028
[St] Status:MEDLINE
[do] DOI:10.1097/SHK.0000000000000516


  8 / 603 MEDLINE  
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[PMID]:26703329
[Au] Autor:Gillies MA; Kakar V; Parker RJ; Honoré PM; Ostermann M
[Ad] Endereço:Department of Anaesthesia, Critical Care & Pain Medicine, Royal Infirmary of Edinburgh, Edinburgh, UK. Michael.Gillies@ed.ac.uk.
[Ti] Título:Fenoldopam to prevent acute kidney injury after major surgery-a systematic review and meta-analysis.
[So] Source:Crit Care;19:449, 2015 Dec 25.
[Is] ISSN:1466-609X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Acute kidney injury (AKI) after surgery is associated with increased mortality and healthcare costs. Fenoldopam is a selective dopamine-1 receptor agonist with renoprotective properties. We conducted a systematic review and meta-analysis of randomised controlled trials comparing fenoldopam with placebo to prevent AKI after major surgery. METHODS: We searched EMBASE, PubMed, meta-Register of randomised controlled trials and Cochrane CENTRAL databases for trials comparing fenoldopam with placebo in patients undergoing major surgery. The primary outcome was incidence of new AKI. Secondary outcomes were requirement for renal replacement therapy and hospital mortality. RESULTS: Eighty-three publications were screened; 23 studies underwent full data extraction and scoring. Six trials were suitable for inclusion in the data synthesis (total of 507 subjects undergoing cardiovascular surgery, partial nephrectomy, liver transplant surgery). Five studies were rated at high risk of bias. Data on post-operative incidence of AKI were available in five of the six trials (total of 471 patients) but definitions of AKI varied between studies. Of the 238 patients receiving fenoldopam, 45 (18.9%) developed AKI compared to 62 (26.6%) of the 233 patients who received placebo (p = 0.004, I (2) = 0 %; random-effects model odds ratio 0.46, 95% confidence interval 0.27-0.79). In patients treated with fenoldopam, there was no difference in renal replacement therapy (n = 478; p = 0.11, I (2) = 47%; fixed-effect model odds ratio 0.27, 95% confidence interval 0.06-1.19) or hospital mortality (p = 0.60, I (2) = 0 %; fixed-effect model odds ratio 1.0, 95% confidence interval 0.14-7.37). CONCLUSIONS: In this analysis, peri-operative treatment with fenoldopam was associated with a significant reduction in post-operative AKI but it had no impact on renal replacement therapy or hospital mortality. Equipoise remains for further large trials in this area since the studies were conducted in three types of surgery, the majority of studies were rated at high risk of bias and the criteria for AKI varied between trials.
[Mh] Termos MeSH primário: Lesão Renal Aguda/prevenção & controle
Fenoldopam/uso terapêutico
[Mh] Termos MeSH secundário: Lesão Renal Aguda/mortalidade
Fenoldopam/administração & dosagem
Fenoldopam/farmacologia
Mortalidade Hospitalar/tendências
Seres Humanos
Procedimentos Cirúrgicos Operatórios/efeitos adversos
Procedimentos Cirúrgicos Operatórios/mortalidade
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
INU8H2KAWG (Fenoldopam)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:160105
[Lr] Data última revisão:
160105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151226
[St] Status:MEDLINE
[do] DOI:10.1186/s13054-015-1166-4


  9 / 603 MEDLINE  
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[PMID]:26242585
[Au] Autor:Liu Y; Xue FS; Li RP
[Ad] Endereço:Department of Anesthesiology, Shanxi Province Tumor Hospital, Taiyuan and Wujiaqu People's Hospital, Wujiaqu City, Xinjiang, People's Republic of China.
[Ti] Título:Intravenous fenoldopam for acute kidney injury.
[So] Source:J Anesth;29(6):979, 2015 Dec.
[Is] ISSN:1438-8359
[Cp] País de publicação:Japan
[La] Idioma:eng
[Mh] Termos MeSH primário: Lesão Renal Aguda/tratamento farmacológico
Fenoldopam/administração & dosagem
Transplante de Fígado/efeitos adversos
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:COMMENT; LETTER
[Nm] Nome de substância:
INU8H2KAWG (Fenoldopam)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150806
[St] Status:MEDLINE
[do] DOI:10.1007/s00540-015-2059-z


  10 / 603 MEDLINE  
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[PMID]:26178154
[Au] Autor:Zhou Y; Shi W; Luo H; Yue R; Wang Z; Wang W; Liu L; Wang WE; Wang H; Zeng C
[Ad] Endereço:Department of Cardiology, Daping Hospital, The Third Military Medical University, Chongqing, China.
[Ti] Título:Inhibitory effect of D1-like dopamine receptors on neuropeptide Y-induced proliferation in vascular smooth muscle cells.
[So] Source:Hypertens Res;38(12):807-12, 2015 Dec.
[Is] ISSN:1348-4214
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Proliferation of vascular smooth muscle cells (VSMCs) is thought to have a key role in the development of atherosclerotic lesions. Neuropeptide Y (NPY), norepinephrine and dopamine are sympathetic neurotransmitters. NPY has been particularly shown to stimulate proliferation of VSMCs. NPY, norepinephrine and dopamine are all sympathetic transmitters. In our previous study, we found that in the presence of the dopamine receptor, the α1-adrenergic receptor-mediated VSMC proliferation is reduced. We hypothesize that the activation of the D1-like receptor might inhibit the NPY-mediated VSMC proliferation. In our present study, we found that NPY, mainly via the Y1 receptor, increased VSMC proliferation. This was determined by [(3)H]-thymidine incorporation, in a concentration (10(-11) to 10(-8) M)-dependent manner. In the presence of the D1-like receptor agonist, fenoldopam (10(-12) to 10(-5) M), the stimulatory effect of NPY on VSMC proliferation was reduced. The involvement of the D1-like receptor was confirmed when the inhibitory effect of fenoldopam was reversed in the presence of the D1-like receptor antagonist SCH-23390 (10(-8) M). Moreover, the inhibitory effect of fenoldopam on NPY-mediated VSMC proliferation was also blocked in the presence of the PKA inhibitor 14-22 (10(-6) M). Protein kinase A activator 8-(4-chlorophenylthio) adenosine-3,5-cyclic monophosphorothioate, Sp-isomer sodium salt (10(-6) M) could simulate the stimulatory effect of fenoldopam. It indicated that the inhibitory effect of D1-like receptors on NPY-mediated VSMC proliferation may have an important role in the regulation of blood pressure or prevention of atherosclerosis.
[Mh] Termos MeSH primário: Músculo Liso Vascular/efeitos dos fármacos
Miócitos de Músculo Liso/efeitos dos fármacos
Neuropeptídeo Y/farmacologia
Receptores de Dopamina D1/fisiologia
[Mh] Termos MeSH secundário: Animais
Aterosclerose/etiologia
Proliferação Celular/efeitos dos fármacos
Proteínas Quinases Dependentes de AMP Cíclico/fisiologia
Fenoldopam/farmacologia
Masculino
Músculo Liso Vascular/citologia
Miócitos de Músculo Liso/fisiologia
Neointima
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Neuropeptide Y); 0 (Receptors, Dopamine D1); EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases); INU8H2KAWG (Fenoldopam)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150717
[St] Status:MEDLINE
[do] DOI:10.1038/hr.2015.84



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