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[PMID]:27384184
[Au] Autor:Sansoè G; Aragno M; Mastrocola R; Mengozzi G; Parola M
[Ad] Endereço:Division of Gastroenterology, Gradenigo Hospital, Torino, Italy.
[Ti] Título:Alpha-2A Adrenoceptor Agonist Guanfacine Restores Diuretic Efficiency in Experimental Cirrhotic Ascites: Comparison with Clonidine.
[So] Source:PLoS One;11(7):e0158486, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: In human cirrhosis, adrenergic hyperfunction causes proximal tubular fluid retention and contributes to diuretic-resistant ascites, and clonidine, a sympatholytic drug, improves natriuresis in difficult-to-treat ascites. AIM: To compare clonidine (aspecific α2-adrenoceptor agonist) to SSP-002021R (prodrug of guanfacine, specific α2A-receptor agonist), both associated with diuretics, in experimental cirrhotic ascites. METHODS AND RESULTS: Six groups of 12 rats were studied: controls (G1); controls receiving furosemide and potassium canrenoate (G2); rats with ascitic cirrhosis due to 14-week CCl4 treatment (G3); cirrhotic rats treated (over the 11th-14th CCl4 weeks) with furosemide and canrenoate (G4), furosemide, canrenoate and clonidine (G5), or diuretics and SSP002021R (G6). Three rats of each group had their hormonal status and renal function assessed at the end of 11th, 12th, 13th, and 14th weeks of respective treatments.Cirrhotic rats in G3 and G4 gained weight over the 12th-14th CCl4 weeks. In G4, brief increase in sodium excretion over the 11th-12th weeks preceded worsening of inulin clearance and natriuresis (diuretic resistance). In comparison with G4, the addition of clonidine (G5) or guanfacine (G6) to diuretics improved, respectively, sodium excretion over the 11th-12th CCl4 weeks, or GFR and electrolytes excretion over the 13th-14th CCl4 weeks. Natriuretic responses in G5 and G6 were accompanied by reduced catecholamine serum levels. CONCLUSIONS: α2A-receptor agonists restore glomerular filtration rate and natriuresis, and delay diuretic-resistant ascites in experimental advanced cirrhosis. Clonidine ameliorates diuretic-dependent natriuresis just for a short time.
[Mh] Termos MeSH primário: Agonistas Adrenérgicos/uso terapêutico
Ascite/tratamento farmacológico
Clonidina/uso terapêutico
Diuréticos/uso terapêutico
Fibrose/tratamento farmacológico
Guanfacina/análogos & derivados
Guanfacina/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Ácido Canrenoico/administração & dosagem
Clonidina/administração & dosagem
Sinergismo Farmacológico
Furosemida/administração & dosagem
Guanfacina/química
Masculino
Ratos
Ratos Wistar
Receptores Adrenérgicos alfa 2/química
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic Agonists); 0 (Diuretics); 0 (Receptors, Adrenergic, alpha-2); 30OMY4G3MK (Guanfacine); 7LXU5N7ZO5 (Furosemide); 87UG89VA9K (Canrenoic Acid); MN3L5RMN02 (Clonidine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160708
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0158486


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[PMID]:27102506
[Au] Autor:Beygui F; Cayla G; Roule V; Roubille F; Delarche N; Silvain J; Van Belle E; Belle L; Galinier M; Motreff P; Cornillet L; Collet JP; Furber A; Goldstein P; Ecollan P; Legallois D; Lebon A; Rousseau H; Machecourt J; Zannad F; Vicaut E; Montalescot G; ALBATROSS Investigators
[Ad] Endereço:ACTION Study Group, Service de Cardiologie, Centre Hospitalier Universitaire de Caen, Caen, France.
[Ti] Título:Early Aldosterone Blockade in Acute Myocardial Infarction: The ALBATROSS Randomized Clinical Trial.
[So] Source:J Am Coll Cardiol;67(16):1917-27, 2016 Apr 26.
[Is] ISSN:1558-3597
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mineralocorticoid receptor antagonists (MRA) improve outcome in the setting of post-myocardial infarction (MI) heart failure (HF). OBJECTIVES: The study sought to assess the benefit of an early MRA regimen in acute MI irrespective of the presence of HF or left ventricular (LV) dysfunction. METHODS: We randomized 1,603 patients to receive an MRA regimen with a single intravenous bolus of potassium canrenoate (200 mg) followed by oral spironolactone (25 mg once daily) for 6 months in addition to standard therapy or standard therapy alone. The primary outcome of the study was the composite of death, resuscitated cardiac arrest, significant ventricular arrhythmia, indication for implantable defibrillator, or new or worsening HF at 6-month follow-up. Key secondary/safety outcomes included death and other individual components of the primary outcome and rates of hyperkalemia at 6 months. RESULTS: The primary outcome occurred in 95 (11.8%) and 98 (12.2%) patients in the treatment and control groups, respectively (hazard ratio [HR]: 0.97; 95% confidence interval [CI]: 0.73 to 1.28). Death occurred in 11 (1.4%) and 17 (2.1%) patients in the treatment and control groups, respectively (HR: 0.65; 95% CI: 0.30 to 1.38). In a non-pre-specified exploratory analysis, the odds of death were reduced in the treatment group (3 [0.5%] vs. 15 [2.4%]; HR: 0.20; 95% CI: 0.06 to 0.70) in the subgroup of ST-segment elevation MI (n = 1,229), but not in non-ST-segment elevation MI (p for interaction = 0.01). Hyperkalemia >5.5 mmol/l(-1) occurred in 3% and 0.2% of patients in the treatment and standard therapy groups, respectively (p < 0.0001). CONCLUSIONS: The study failed to show the benefit of early MRA use in addition to standard therapy in patients admitted for MI. (Aldosterone Lethal effects Blockade in Acute myocardial infarction Treated with or without Reperfusion to improve Outcome and Survival at Six months follow-up; NCT01059136).
[Mh] Termos MeSH primário: Ácido Canrenoico/administração & dosagem
Insuficiência Cardíaca/tratamento farmacológico
Antagonistas de Receptores de Mineralocorticoides/uso terapêutico
Infarto do Miocárdio/tratamento farmacológico
Espironolactona/administração & dosagem
Disfunção Ventricular Esquerda/tratamento farmacológico
[Mh] Termos MeSH secundário: Fatores Etários
Idoso
Quimioterapia Combinada
Eletrocardiografia/métodos
Feminino
Seguimentos
Insuficiência Cardíaca/diagnóstico
Insuficiência Cardíaca/mortalidade
Seres Humanos
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Infarto do Miocárdio/diagnóstico
Infarto do Miocárdio/mortalidade
Modelos de Riscos Proporcionais
Medição de Risco
Índice de Gravidade de Doença
Fatores Sexuais
Método Simples-Cego
Estatísticas não Paramétricas
Análise de Sobrevida
Fatores de Tempo
Resultado do Tratamento
Disfunção Ventricular Esquerda/diagnóstico
Disfunção Ventricular Esquerda/mortalidade
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; MULTICENTER STUDY; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mineralocorticoid Receptor Antagonists); 27O7W4T232 (Spironolactone); 87UG89VA9K (Canrenoic Acid)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:160422
[Lr] Data última revisão:
160422
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160423
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE


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[PMID]:26519424
[Au] Autor:Sansoè G; Aragno M; Mastrocola R; Parola M
[Ad] Endereço:Division of Gastroenterology, Gradenigo Hospital, 10135 Torino, Italy giovannisan@iol.it.
[Ti] Título:Pathogenesis of solute-free water retention in experimental ascitic cirrhosis: is vasopressin the only culprit?
[So] Source:Clin Sci (Lond);130(2):117-24, 2016 Jan.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Catecholamines trigger proximal tubular fluid retention and reduce renal excretion of solute-free water. In advanced cirrhosis, non-osmotic hypersecretion of vasopressin (antidiuretic hormone or ADH) is considered the cause of dilutional hyponatraemia, but ADH V2 receptor antagonists are not beneficial in long-term treatment of ascites. To test the hypothesis that water retention in experimental ascitic cirrhosis might depend primarily on adrenergic hyper-function, hormonal status, renal function and tubular free-water reabsorption (TFWR) were assessed in six groups of rats with ascitic cirrhosis: rats with cirrhosis due to 13-week CCl4 (carbon tetrachloride) administration (group G1); cirrhotic rats receiving daily diuretics (0.5 mg/kg furosemide plus 2 mg/kg K(+)-canrenoate) from the 11th to the 13th week of CCl4 (G2), diuretics associated with guanfacine oral prodrug (α2A-adrenergic receptor agonist and sympatholytic agent) at 2 (G3), 7 (G4) or 10 (G5) mg/kg, or with SSP-004240F1 (V2 receptor antagonist) at 1 mg/kg (G6). Natriuresis was lower in G1 than in G2, G4 and G6 (all P<0.05). Guanfacine, added to diuretics (i.e. G3 compared with G2), reduced serum noradrenaline from 423±22 to 211±41 ng/l (P<0.05), plasma renin activity (PRA) from 35±8 to 9±2 ng/ml/h (P<0.05) and TFWR from 45±8 to 20±6 µl/min (P<0.01). TFWR correlated with plasma aldosterone (r=0.51, P<0.01) and urinary potassium excretion (r=0.90, P<0.001). In ascitic cirrhosis, reduced volaemia, use of diuretics (especially furosemide) and adrenergic hyper-function cause tubular retention of water. Suitable doses of sympatholytic agents are effective aquaretics.
[Mh] Termos MeSH primário: Ascite/fisiopatologia
Cirrose Hepática Experimental/fisiopatologia
Vasopressinas/fisiologia
[Mh] Termos MeSH secundário: Animais
Ascite/tratamento farmacológico
Ascite/etiologia
Ácido Canrenoico/farmacologia
Diuréticos/farmacologia
Furosemida/farmacologia
Guanfacina/farmacologia
Hiponatremia/etiologia
Hiponatremia/fisiopatologia
Cirrose Hepática Experimental/complicações
Masculino
Natriurese/efeitos dos fármacos
Natriurese/fisiologia
Norepinefrina/sangue
Ratos
Ratos Wistar
Vasopressinas/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Diuretics); 11000-17-2 (Vasopressins); 30OMY4G3MK (Guanfacine); 7LXU5N7ZO5 (Furosemide); 87UG89VA9K (Canrenoic Acid); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:151215
[Lr] Data última revisão:
151215
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151101
[St] Status:MEDLINE
[do] DOI:10.1042/CS20150479


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[PMID]:25389106
[Au] Autor:Alexandre J; Beygui F; Puddu PE; Manrique A; Rouet R; Milliez P
[Ad] Endereço:Department of Cardiology, CHU de Caen, Caen, France Université de Caen Basse-Normandie, EA 4650 Signalisation, électrophysiologie et imagerie des lésions d'ischémie-reperfusion myocardique, Caen, France alexandre-j@chu-caen.fr.
[Ti] Título:Electrophysiological and antiarrhythmic properties of potassium canrenoate during myocardial ischemia-reperfusion.
[So] Source:J Cardiovasc Pharmacol Ther;20(3):313-21, 2015 May.
[Is] ISSN:1940-4034
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Recent clinical studies have reported the potential benefit of an early mineralocorticoid receptor (MR) blockade with potassium canrenoate (PC) on ventricular arrhythmias (VAs) occurrence in patients experiencing an ST-segment elevation myocardial infarction (STEMI). However, most of the electrophysiological properties of PC demonstrated to date have been investigated in normoxic conditions, and therefore, in vitro experiments during an acute myocardial ischemia-reperfusion were lacking. MATERIALS AND METHODS: We used rabbit in vitro models and standard microelectrode technique to assess the electrophysiological impact of PC during myocardial ischemia-reperfusion, including right ventricle mimicking the "border zone" existing between normal and ischemic/reperfused areas (1 µmol/L, 10 and 100 nmol/L), isolated right ventricle, and sinoatrial node (SAN) experiments (1 µmol/L, respectively). RESULTS: During ischemia-reperfusion, acute superfusion of PC 100 nmol/L prevented the increase in action potential (AP) duration at 90% of repolarization (APD90) dispersion between ischemic and nonischemic areas and in VAs occurrence induced by aldosterone 10 nmol/L (86 ± 3 vs 114 ± 4 milliseconds for aldosterone alone, P < .05). Potassium canrenoate also induced conduction blocks and significantly decreased Vmax during simulated ischemia (from 25 ± 5 to 12 ± 4, 14 ± 3, and 14 ± 5 V/s, respectively, for PC 1 µmol/L, 100, and 10 nmol/L, P < .05). Potassium canrenoate 1 µmol/L demonstrated cycle length (CL)-dependent effects on APD90 and on Vmax, and it also reduced SAN beating CL (from 446 ± 28 to 529 ± 24 millisecond, P < .05). CONCLUSION: Our experimental study highlights new evidence for an antiarrhythmic impact of PC during myocardial ischemia-reperfusion via multiple channels modulation. These results are in line with recent clinical trials suggesting that an early MR blockade in STEMI may be preventive of VAs.
[Mh] Termos MeSH primário: Antiarrítmicos/farmacologia
Ácido Canrenoico/farmacologia
Antagonistas de Receptores de Mineralocorticoides/farmacologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Feminino
Masculino
Reperfusão Miocárdica
Coelhos
Nó Sinoatrial/efeitos dos fármacos
Nó Sinoatrial/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Mineralocorticoid Receptor Antagonists); 87UG89VA9K (Canrenoic Acid)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:150416
[Lr] Data última revisão:
150416
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141113
[St] Status:MEDLINE
[do] DOI:10.1177/1074248414557036


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[PMID]:23539659
[Au] Autor:Rossi R; Crupi N; Coppi F; Monopoli D; Sgura F
[Ad] Endereço:Institute of Cardiology, Policlinico Hospital, University of Modena and Reggio Emilia, Italy rossi.rosario@unimore.it.
[Ti] Título:Importance of the time of initiation of mineralocorticoid receptor antagonists on risk of mortality in patients with heart failure.
[So] Source:J Renin Angiotensin Aldosterone Syst;16(1):119-25, 2015 Mar.
[Is] ISSN:1752-8976
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Several studies have definitively shown the benefit of mineralocorticoid receptor antagonists (MRAs) in patients with heart failure (HF). However, very few prior studies examined the relationship between the timing of initiation of MRAs and prognosis. In addition, on this topic, there is no information regarding the specific population of patients suffering a first episode of decompensated congestive HF. METHODS: We studied a homogenous cohort of patients discharged alive from our hospital after a first episode of decompensated congestive HF, in order to clarify the association between time of aldosterone receptor antagonist (ARA) initiation (within the first 90 days after hospital discharge) and mortality. Our population was composed of a series of consecutive patients. All-cause mortality was compared between patients who initiated MRAs at discharge (early group) and those who initiated MRAs one month later and up to 90 days after discharge (delayed group). We used prescription time distribution matching to control for survival difference between groups. RESULTS: The early and delayed groups consisted of 365 and 320 patients, respectively. During the one-year follow-up, a significant difference in mortality was demonstrated between groups. Adjusted hazard ratios (HRs) for early versus delayed initiation were 1.72 (95% confidence interval (CI) 0.96 to 2.84) at six months, and 1.93 (95% CI 1.18 to 3.14) at one year. CONCLUSIONS: Delay of MRA initiation up to 30 to 90 days after discharge implies a significant increase in mortality compared with MRA initiation at discharge, after a first episode of decompensate congestive HF.
[Mh] Termos MeSH primário: Insuficiência Cardíaca/tratamento farmacológico
Insuficiência Cardíaca/mortalidade
Antagonistas de Receptores de Mineralocorticoides/uso terapêutico
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Ácido Canrenoico/uso terapêutico
Estudos de Coortes
Feminino
Seguimentos
Seres Humanos
Masculino
Meia-Idade
Prognóstico
Espironolactona/uso terapêutico
Análise de Sobrevida
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Mineralocorticoid Receptor Antagonists); 27O7W4T232 (Spironolactone); 87UG89VA9K (Canrenoic Acid)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:150422
[Lr] Data última revisão:
150422
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130330
[St] Status:MEDLINE
[do] DOI:10.1177/1470320313482603


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[PMID]:24423282
[Au] Autor:Iqbal J; Andrew R; Cruden NL; Kenyon CJ; Hughes KA; Newby DE; Hadoke PW; Walker BR
[Ad] Endereço:University/BHF Centre for Cardiovascular Science, University of Edinburgh, Edinburgh EH16 4TJ, United Kingdom.
[Ti] Título:Displacement of cortisol from human heart by acute administration of a mineralocorticoid receptor antagonist.
[So] Source:J Clin Endocrinol Metab;99(3):915-22, 2014 Mar.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:CONTEXT: Mineralocorticoid receptor (MR) antagonists have beneficial effects in patients with heart failure and myocardial infarction, often attributed to blocking aldosterone action in the myocardium. However, binding of aldosterone to MR requires local activity of the enzyme 11ß-hydroxysteroid dehydrogenase type 2 (11ß-HSD2), which inactivates cortisol to cortisone and thereby prevents receptor occupancy by cortisol. In vivo activity of 11ß-HSD2 and potential occupancy of MR by cortisol in human heart have not been quantified. OBJECTIVE: This study aimed to measure in vivo activity of 11ß-HSD2 and to establish whether cortisol binds MR in human heart. PARTICIPANTS AND INTERVENTIONS: Nine patients without heart failure undergoing diagnostic coronary angiography were infused to steady state with the stable isotope tracers 9,11,12,12-[(2)H]4-cortisol and 1,2-[(2)H]2-cortisone to quantify cortisol and cortisone production. Samples were obtained from the femoral artery and coronary sinus before and for 40 minutes after bolus iv administration of an MR antagonist, potassium canrenoate. Coronary sinus blood flow was measured by venography and Doppler flow wire. RESULTS: There was no detectable production of cortisol or cortisone across the myocardium. After potassium canrenoate administration, plasma aldosterone concentrations increased substantially but aldosterone was not detectably released from the myocardium. In contrast, plasma cortisol concentrations did not change in the systemic circulation but tissue-bound cortisol was released transiently from the myocardium after potassium canrenoate administration. CONCLUSIONS: Human cardiac 11ß-HSD2 activity appears too low to inactivate cortisol to cortisone. Cortisol is displaced acutely from the myocardium by MR antagonists and may contribute to adverse MR activation in human heart.
[Mh] Termos MeSH primário: Ácido Canrenoico/administração & dosagem
Coração/efeitos dos fármacos
Hidrocortisona/metabolismo
Antagonistas de Receptores de Mineralocorticoides/administração & dosagem
Miocárdio/metabolismo
[Mh] Termos MeSH secundário: 11-beta-Hidroxiesteroide Desidrogenase Tipo 2/metabolismo
Idoso
Cortisona/metabolismo
Esquema de Medicação
Feminino
Seres Humanos
Masculino
Meia-Idade
Miocárdio/enzimologia
Receptores de Mineralocorticoides/metabolismo
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mineralocorticoid Receptor Antagonists); 0 (Receptors, Mineralocorticoid); 87UG89VA9K (Canrenoic Acid); EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenase Type 2); V27W9254FZ (Cortisone); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:140116
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2013-2049


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[PMID]:23846862
[Au] Autor:Suyagh M; Hawwa AF; Collier PS; Millership JS; Kole P; Millar M; Shields MD; Halliday HL; McElnay JC
[Ad] Endereço:aClinical & Practice Research Group, School of Pharmacy bRegional Neonatal Unit, Royal Maternity Hospital and Department of Child Health cRoyal Belfast Hospital for Sick Children, Belfast Health and Social Care Trust and Institute of Clinical Research, Queen's University Belfast, Belfast, UK.
[Ti] Título:Potassium canrenoate treatment in paediatric patients: a population pharmacokinetic study using novel dried blood spot sampling.
[So] Source:J Hypertens;31(9):1901-8, 2013 Sep.
[Is] ISSN:1473-5598
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: To characterize the population pharmacokinetics of canrenone following administration of potassium canrenoate (K-canrenoate) in paediatric patients. METHODS: Data were collected prospectively from 37 paediatric patients (median weight 2.9 kg, age range 2 days-0.85 years) who received intravenous K-canrenoate for management of retained fluids, for example in heart failure and chronic lung disease. Dried blood spot (DBS) samples (n=213) from these were analysed for canrenone content and the data subjected to pharmacokinetic analysis using nonlinear mixed-effects modelling. Another group of patients (n=16) who had 71 matching plasma and DBS samples was analysed separately to compare canrenone pharmacokinetic parameters obtained using the two different matrices. RESULTS: A one-compartment model best described the DBS data. Significant covariates were weight, postmenstrual age (PMA) and gestational age. The final population models for canrenone clearance (CL/F) and volume of distribution (V/F) in DBS were CL/F (l/h) = 12.86 ×  (WT/70.0) × e [0.066 ×  (PMA - 40]) and V/F (l) = 603.30 ×  (WT/70) × (GA/40) where weight is in kilograms. The corresponding values of CL/F and V/F in a patient with a median weight of 2.9 kg are 1.11 l/h and 20.48 l, respectively. Estimated half-life of canrenone based on DBS concentrations was similar to that based on matched plasma concentrations (19.99 and 19.37 h, respectively, in 70 kg patient). CONCLUSION: The range of estimated CL/F in DBS for the study population was 0.12-9.62 l/h; hence, bodyweight-based dosage adjustment of K-canrenoate appears necessary. However, a dosing scheme that takes into consideration both weight and age (PMA/gestational age) of paediatric patients seems more appropriate.
[Mh] Termos MeSH primário: Ácido Canrenoico/farmacocinética
Ácido Canrenoico/uso terapêutico
Teste em Amostras de Sangue Seco/métodos
[Mh] Termos MeSH secundário: Administração Intravenosa
Peso Corporal
Simulação por Computador
Esquema de Medicação
Feminino
Idade Gestacional
Insuficiência Cardíaca/sangue
Insuficiência Cardíaca/tratamento farmacológico
Seres Humanos
Lactente
Recém-Nascido
Pneumopatias/sangue
Pneumopatias/tratamento farmacológico
Masculino
Estudos Prospectivos
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
87UG89VA9K (Canrenoic Acid)
[Em] Mês de entrada:1405
[Cu] Atualização por classe:131010
[Lr] Data última revisão:
131010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130713
[St] Status:MEDLINE
[do] DOI:10.1097/HJH.0b013e3283626994


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[PMID]:23785077
[Au] Autor:Feng X; Reini SA; Richards E; Wood CE; Keller-Wood M
[Ad] Endereço:Departments of Pharmacodynamics, and Physiology and Functional Genomics, University of Florida, Gainesville, Florida.
[Ti] Título:Cortisol stimulates proliferation and apoptosis in the late gestation fetal heart: differential effects of mineralocorticoid and glucocorticoid receptors.
[So] Source:Am J Physiol Regul Integr Comp Physiol;305(4):R343-50, 2013 Aug 15.
[Is] ISSN:1522-1490
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have previously found that modest chronic increases in maternal cortisol result in an enlarged fetal heart. To explore the mechanisms of this effect, we used intrapericardial infusions of a mineralocorticoid receptor (MR) antagonist (canrenoate) or of a glucocorticoid receptor (GR) antagonist (mifepristone) in the fetus during maternal infusion of cortisol (1 mg·kg⁻¹·day⁻¹). We have shown that the MR antagonist blocked the increase in fetal heart weight and in wall thickness resulting from maternal cortisol infusion. In the current study we extended those studies and found that cortisol increased Ki67 staining in both ventricles, indicating cell proliferation, but also increased active caspase-3 staining in cells of the conduction pathway in the septum and subendocardial layers of the left ventricle, suggesting increased apoptosis in Purkinje fibers. The MR antagonist blocked the increase in cell proliferation, whereas the GR antagonist blocked the increased apoptosis in Purkinje fibers. We also found evidence of activation of caspase-3 in c-kit-positive cells, suggesting apoptosis in stem cell populations in the ventricle. These studies suggest a potentially important role of corticosteroids in the terminal remodeling of the late gestation fetal heart and suggest a mechanism for the cardiac enlargement with excess corticosteroid exposure.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Coração Fetal/efeitos dos fármacos
Hidrocortisona/farmacologia
Receptores de Glucocorticoides/efeitos dos fármacos
Receptores de Mineralocorticoides/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Ácido Canrenoico/farmacologia
Cardiomegalia/induzido quimicamente
Cardiomegalia/metabolismo
Cardiomegalia/patologia
Caspase 3/metabolismo
Feminino
Coração Fetal/metabolismo
Coração Fetal/patologia
Idade Gestacional
Hidrocortisona/administração & dosagem
Hidrocortisona/toxicidade
Infusões Intravenosas
Antígeno Ki-67/metabolismo
Mifepristona/farmacologia
Antagonistas de Receptores de Mineralocorticoides/farmacologia
Gravidez
Proteínas Proto-Oncogênicas c-kit/metabolismo
Ramos Subendocárdicos/efeitos dos fármacos
Ramos Subendocárdicos/metabolismo
Ramos Subendocárdicos/patologia
Receptores de Glucocorticoides/metabolismo
Receptores de Mineralocorticoides/metabolismo
Ovinos
Células-Tronco/efeitos dos fármacos
Células-Tronco/metabolismo
Células-Tronco/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ki-67 Antigen); 0 (Mineralocorticoid Receptor Antagonists); 0 (Receptors, Glucocorticoid); 0 (Receptors, Mineralocorticoid); 320T6RNW1F (Mifepristone); 87UG89VA9K (Canrenoic Acid); EC 2.7.10.1 (Proto-Oncogene Proteins c-kit); EC 3.4.22.- (Caspase 3); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1310
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130621
[St] Status:MEDLINE
[do] DOI:10.1152/ajpregu.00112.2013


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[PMID]:23753530
[Au] Autor:Rademaker MT; Charles CJ; Nicholls MG; Richards AM
[Ad] Endereço:Christchurch Heart Institute, Department of Medicine, University of Otago-Christchurch, Christchurch, New Zealand. miriam.rademaker@otago.ac.nz
[Ti] Título:Interactions of enhanced urocortin 2 and mineralocorticoid receptor antagonism in experimental heart failure.
[So] Source:Circ Heart Fail;6(4):825-32, 2013 Jul.
[Is] ISSN:1941-3297
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Mineralocorticoid receptor antagonists (MRAs) have become established therapy in heart failure (HF). Urocortin 2 (Ucn2) is a novel peptide with potential in the treatment of this disease. The present study investigated the interactions of acute administration of Ucn2 and an MRA in experimental HF. METHODS AND RESULTS: Ucn2 and an MRA (canrenoic acid [CA]) were infused for 4 hours, both singly and together, in 8 sheeps with pacing-induced HF. Ucn2, when administered as an adjunct to CA, further improved hemodynamic indices relative to that achieved by CA alone, producing additional increases in cardiac output and decreases in left atrial pressure and peripheral resistance but without eliciting a supplementary reduction in arterial pressure. Ucn2 cotreatment reversed CA-induced rises in circulating aldosterone levels, and also significantly reduced plasma renin activity, angiotensin II, and vasopressin concentrations. Although both CA and Ucn2 infusion produced a diuresis and natriuresis, responses with Ucn2 and Ucn+CA were 2- to 3-fold greater than that elicited by separate CA. Ucn2 cotherapy additionally increased urine potassium and creatinine excretion. In contrast to the rise in plasma potassium induced by CA, Ucn2 cotreatment reduced potassium concentrations. CONCLUSIONS: Ucn2 cotreatment with an MRA in HF further improved hemodynamics relative to that achieved by CA alone, while also reducing plasma renin activity, angiotensin II, aldosterone and vasopressin levels, and enhancing renal function. Importantly, Ucn2 prevented CA-induced rises in plasma potassium. These data demonstrate a favorable profile of effects with short-term adjunct Ucn2 therapy and an MRA in HF.
[Mh] Termos MeSH primário: Ácido Canrenoico/farmacologia
Insuficiência Cardíaca/fisiopatologia
Antagonistas de Receptores de Mineralocorticoides/farmacologia
Urocortinas/farmacologia
[Mh] Termos MeSH secundário: Animais
Ácido Canrenoico/administração & dosagem
Estimulação Cardíaca Artificial
Interações Medicamentosas
Epinefrina/sangue
Feminino
Insuficiência Cardíaca/tratamento farmacológico
Insuficiência Cardíaca/metabolismo
Hemodinâmica/efeitos dos fármacos
Hidrocortisona/sangue
Antagonistas de Receptores de Mineralocorticoides/administração & dosagem
Norepinefrina/sangue
Potássio/urina
Sistema Renina-Angiotensina/efeitos dos fármacos
Ovinos
Sódio/urina
Urocortinas/administração & dosagem
Urocortinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mineralocorticoid Receptor Antagonists); 0 (Urocortins); 87UG89VA9K (Canrenoic Acid); 9NEZ333N27 (Sodium); RWP5GA015D (Potassium); WI4X0X7BPJ (Hydrocortisone); X4W3ENH1CV (Norepinephrine); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1309
[Cu] Atualização por classe:131121
[Lr] Data última revisão:
131121
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130612
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCHEARTFAILURE.112.000205


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[PMID]:23427921
[Au] Autor:Siddique YH; Ara G; Afzal M
[Ad] Endereço:Drosophila Transgenics Laboratory, Section of Genetics, Department of Zoology, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, U.P., 202002, India. yasir_hasansiddique@rediffmail.com
[Ti] Título:Effect of the steroid K-canrenoate on hsp70 expression and tissue damage in transgenic Drosophila melanogaster (hsp70-lacZ) Bg9.
[So] Source:J Insect Sci;12:92, 2012.
[Is] ISSN:1536-2442
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In the present study the effect of 0.1, 0.2, 0.4, 0.8, and 1.0 µL/mL of the steroid K-canrenoate was evaluated in the third instar larvae of transgenic Drosophila melanogaster (hsp70-lacZ) Bg(9) for 6, 24, and 48 hours of duration. The treatment of 0.1, 0.2, and 0.4 µL/mL of K-canrenoate did not induce the activity of hsp70 significantly compared to the control. The treatments of 0.8 and 1.0 µL/mL of K-canrenoate not only caused tissue damage but also induced a significant increase in the expression of hsp70 for the different durations of exposure. The results of the present study suggest that the K-canrenoate at 0.8 and 1.0 µL/mL is cytotoxic and caused tissue damage in the third instar larvae of transgenic D. melanogaster (hsp70-lacZ) Bg(9).
[Mh] Termos MeSH primário: Ácido Canrenoico/farmacologia
Drosophila melanogaster/efeitos dos fármacos
Antagonistas de Receptores de Mineralocorticoides/farmacologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados/genética
Animais Geneticamente Modificados/metabolismo
Corantes/metabolismo
Relação Dose-Resposta a Droga
Proteínas de Drosophila/genética
Proteínas de Drosophila/metabolismo
Drosophila melanogaster/genética
Drosophila melanogaster/crescimento & desenvolvimento
Regulação da Expressão Gênica/efeitos dos fármacos
Proteínas de Choque Térmico HSP70/genética
Proteínas de Choque Térmico HSP70/metabolismo
Larva/efeitos dos fármacos
Larva/genética
Larva/crescimento & desenvolvimento
Espectrofotometria Atômica
Estresse Fisiológico
Fatores de Tempo
Distribuição Tecidual
Azul Tripano/metabolismo
beta-Galactosidase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Coloring Agents); 0 (Drosophila Proteins); 0 (HSP70 Heat-Shock Proteins); 0 (Mineralocorticoid Receptor Antagonists); 87UG89VA9K (Canrenoic Acid); EC 3.2.1.23 (beta-Galactosidase); I2ZWO3LS3M (Trypan Blue)
[Em] Mês de entrada:1307
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130223
[St] Status:MEDLINE
[do] DOI:10.1673/031.012.9201



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