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Nanoporous gold (NPG) structures were prepared on the surface of a gold microelectrode (Au-µE) by an anodization-reduction method. Cyclic voltammetry and field emission scanning electron microscopy were used to study the electrochemical properties and the morphology of the nanostructured film. Voltammetry showed an improved sensitivity for dopamine (DA) oxidation at this microelectrode when compared to a bare gold microelectrode, with a peak near 0.2 V (vs. Ag/AgCl) at a scan rate of 0.1 V s-1. This is due to the increased surface area and roughness. Square wave voltammetry shows a response that is linear in the 0.1-10 µmol L-1 DA concentration range, with a 30 nmol L-1 detection limit and a sensitivity of 1.18 mA (µmol L-1)-1 cm-2. The sensor is not interfered by ascorbic acid. The reproducibility, repeatability, long-term stability and real sample analysis (spiked urine) were assessed, and acceptable performance was achieved. The "proof-of-concept" detection of dopamine release was demonstrated by using scanning electrochemical microscopy (SECM) with the aim of future applications for single cell analysis. Graphical abstract A reproducible electrochemical approach was proposed to fabricate an NPG-microelectrode for DA detection, with enhanced sensitivity and selectivity. Besides, a proof-of-concept detection of DA release was also demonstrated by using SECM.

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The aim of this study was to demonstrate the effects of atrial natriuretic peptide (ANP) on organic cation transporters (OCTs) expression and activity, and its consequences on dopamine urinary levels, Na+, K+-ATPase activity and renal function. Male Sprague Dawley rats were infused with isotonic saline solution during 120 minutes and randomized in nine different groups: control, pargyline plus tolcapone (P+T), ANP, dopamine (DA), D-22, DA+D-22, ANP+D-22, ANP+DA and ANP+DA+D-22. Renal functional parameters were determined and urinary dopamine concentration was quantified by HPLC. Expression of OCTs and D1-receptor in membrane preparations from renal cortex tissues were determined by western blot and Na+, K+-ATPase activity was determined using in vitro enzyme assay. 3H-DA renal uptake was determined in vitro. Compared to P+T group, ANP and dopamine infusion increased diuresis, urinary sodium and dopamine excretion significantly. These effects were more pronounced in ANP+DA group and reversed by OCTs blockade by D-22, demonstrating that OCTs are implied in ANP stimulated-DA uptake and transport in renal tissues. The activity of Na+, K+-ATPase exhibited a similar fashion when it was measured in the same experimental groups. Although OCTs and D1-receptor protein expression were not modified by ANP, OCTs-dependent-dopamine tubular uptake was increased by ANP through activation of NPR-A receptor and protein kinase G as signaling pathway. This effect was reflected by an increase in urinary dopamine excretion, natriuresis, diuresis and decreased Na+, K+-ATPase activity. OCTs represent a novel target that links the activity of ANP and dopamine together in a common mechanism to enhance their natriuretic and diuretic effects.

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This paper describes the synthesis, characterization and applications of a new hybrid material composed of mesoporous silica (SiO2) modified with graphene oxide (GO), SiO2/GO, obtained by the sol-gel process using HF as the catalyst. The hybrid material, SiO2/GO, was decorated with silver nanoparticles (AgNPs) with a size of less than 20 nanometres, prepared directly on the surface of the material using N,N-dimethylformamide (DMF) as the reducing agent. The resulting material was designated as AgNP/SiO2/GO. The Ag/SiO2/GO material was characterized by X-ray photoelectron spectroscopy (XPS), scanning electron microscopy (SEM), energy-dispersive X-ray (EDX) and high-resolution transmission electron microscopy (HR-TEM). A glassy carbon electrode modified with AgNP/SiO2/GO was used in the development of a sensitive electrochemical sensor for the simultaneous determination of epinephrine and dopamine employing electrocatalytic reduction using squarewave voltammetry. Well-defined and separate reduction peaks were observed in PBS buffer at pH 7. No significant interference was seen for primarily biological interferents such as uric acid and ascorbic acid in the detection of dopamine and epinephrine. Our study demonstrated that the resultant AgNP/SiO2/GO-modified electrode is highly sensitive for the simultaneous determination of dopamine and epinephrine, with the limits of detection being 0.26 and 0.27 µmol L(-1), respectively. The AgNP/SiO2/GO-modified electrode is highly selective and can be used to detect dopamine and epinephrine in a human urine sample.

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Diuretic and natriuretic effects of renal dopamine (DA) are well established. However, in volume expansion the pattern of renal DA release into urine (UDAV) and the role of enzymes involved in DA synthesis/degradation have not yet been defined. The objective was to determine the pattern of UDAV during volume expansion and to characterize the involvement of monoamine-oxidase (MAO) and aromatic amino-acid decarboxylase (AADC) in this response. In this study male Wistar rats were expanded with NaCl 0.9% at a rate of 5% BWt per hour. At the beginning of expansion three groups received a single drug injection as follows: C (vehicle, Control), IMAO (MAO inhibitor Pargyline, 20 mg/kg BWt, i.v.) and BNZ (AADC inhibitor Benserazide, 25 mg/kg BWt, i.v.). Results revealed that in C rats UDAV (ng/30 min/100g BWt) increased in the first 30 min expansion from 11.5 +/- 1.20 to 21.8 +/- 3.10 (p < 0.05) and decreased thereafter. IMAO showed a similar pattern but significantly higher than C at 30 min expansion (32.5 +/- 2.20, p < 0.05). IMAO greatly reduced MAO activity from 8.29 +/- 0.35 to 1.1 +/- 0.03 nmol/mg tissue/hour and significantly increased diuresis and natriuresis over controls. BNZ abolished the early UDAV peak to 3.2+/-0.72 (p < 0.01) and though, UDAV increased over C after 60 min expansion, natriuresis and diuresis were diminished by BNZ treatment. Results indicate that an increment in renal DA release into urine occurs early in expansion and in a peak-shaped way. In this response MAO plays a predominant role.

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Diuretic and natriuretic effects of renal dopamine (DA) are well established. However, in volume expansion the pattern of renal DA release into urine (U DA V) and the role of enzymes involved in DA synthesis/degradation have not yet been defined. The objective was to determine the pattern of U DA V during volume expansion and to characterize the involvement of monoamine-oxidase (MAO) and aromatic amino-acid decarboxylase (AADC) in this response. In this study male Wistar rats were expanded with NaCl 0.9% at a rate of 5% BWt per hour. At the beginning of expansion three groups received a single drug injection as follows: C (vehicle, Control), IMAO (MAO inhibitor Pargyline, 20 mg/kg BWt, i.v.) and BNZ (AADC inhibitor Benserazide, 25 mg/kg BWt, i.v.). Results revealed that in C rats U DA V (ng/30 min/100g BWt) increased in the first 30 min expansion from 11.5 ± 1.20 to 21.8 ± 3.10 (p < 0.05) and decreased thereafter. IMAO showed a similar pattern but significantly higher than C at 30 min expansion (32.5 ± 2.20, p < 0.05). IMAO greatly reduced MAO activity from 8.29 ± 0.35 to 1.1 ± 0.03 nmol/mg tissue/hour and significantly increased diuresis and natriuresis over controls. BNZ abolished the early U DA V peak to 3.2±0.72 (p < 0.01) and though, U DA V increased over C after 60 min expansion, natriuresis and diuresis were diminished by BNZ treatment. Results indicate that an increment in renal DA release into urine occurs early in expansion and in a peak-shaped way. In this response MAO plays a predominant role.

La dopamina (DA) intrarrenal ejerce efectos diuréticos y natriuréticos. Sin embargo, en los estado de expansión de volumen aún no está bien definido el patrón de liberación de dopamina renal hacia la orina y si cumplen un rol las enzimas involucradas en la síntesis o degradación de la amina. El objetivo del presente trabajo fue determinar el patrón de excreción urinaria de DA (U DA V) durante la expansión de volumen, caracterizando la participación de las enzimas monoaminooxidasa (MAO) y decarboxilasa de aminoácidos aromáticos (AADC) en esta respuesta. Para ello ratas Wistar macho fueron expandidas de volumen con NaCl 0.9% al 5% del peso corporal por hora durante dos horas y divididas en tres grupos, los que al comienzo de la expansión recibieron: C (vehículo, Control), IMAO (Pargilina, inhibidor de MAO, 20 mg/kg PC, i.v.) y BNZ (Benserazida, inhibidor de AADC, 25 mg/kg PC, i.v.). Se observó que en C la U DA V (ng/30min/100gPC) aumentó durante los primeros 30 minutos de expansión de 11.5 ± 1.20 a 21.8 ± 3.10 (p < 0.05), disminuyendo posteriormente. IMAO mostró un patrón de liberación similar pero significativamente mayor que C a los 30 min de expansión (32.5 ± 2.20, p < 0.05). En este grupo la actividad de MAO disminuyó de 8.29 ± 0.35 a 1.1 ± 0.03 nmol/mg tejido/hora y aumentaron la diuresis y natriuresis por sobre los controles. En BNZ, el pico de U DA V observado a los 30 min de la expansión disminuyó a 3.2 ± 0.72 (p < 0.01), aunque luego de 60 minutos fue mayor que en C. BNZ disminuyó tanto la diuresis como la natriuresis. Podemos concluir que al comienzo de la expansión de volumen se produce un pico de excreción de dopamina renal hacia la orina. La enzima MAO juega un rol fundamental en esta respuesta.

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INTRODUCTION: Sleep bruxism (SB) is characterized by repetitive and coordinated mandible movements and non-functional teeth contacts during sleep time. Although the etiology of SB is controversial, the literature converges on its multifactorial origin. Occlusal factors, smoking, alcoholism, drug usage, stress, and anxiety have been described as SB trigger factors. Recent studies on this topic discussed the role of neurotransmitters on the development of SB. OBJECTIVE: Thus, the purpose of this study was to detect and quantify the urinary levels of catecholamines, specifically of adrenaline, noradrenaline and dopamine, in subjects with SB and in control individuals. MATERIALS AND METHODS: Urine from individuals with SB (n = 20) and without SB (n = 20) was subjected to liquid chromatography. The catecholamine data were compared by Mann-Whitney's test (p

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Atrial natriuretic factor (ANF) and dopamine (DA) are both important regulators of sodium and water transport across renal proximal tubules. Many evidences suggest that some of ANF inhibitory effects on sodium and water reabsorption are mediated by dopaminergic mechanisms. We have previously reported that ANF stimulates extraneuronal DA uptake in external renal cortex by activation of NPR-A receptors coupled to cGMP signal and PKG. Moreover, ANF enhanced DA-induced inhibition of Na(+)-K(+) ATPase activity. The aim of the present study was to evaluate if ANF could alter also renal DA release, catabolism and turn over. The results indicate that ANF did not affect basal secretion of the amine in external renal cortex or its KCl-induced release, but diminished DA turn over. Moreover, ANF diminished COMT and did not alter MAO activity. In conclusion, present results as well as previous findings show that ANF modifies DA metabolism in rat external renal cortex by enhancing DA uptake and decreasing COMT activity. All those effects, taken together, may favor DA accumulation into renal cells and increase its endogenous content and availability. This would permit D1 receptor recruitment and stimulation and in turn, Na(+), K(+)-ATPase activity over inhibition that results in decreased sodium reabsorption. Therefore, ANF and DA could act via a common pathway to enhance natriuresis and diuresis.

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AIMS: The interplay between natriuretic dopamine and antinatriuretic angiotensin II represents an important mechanism for the regulation of renal sodium and water excretion. Monoamine oxidase is the main metabolizing pathway for dopamine in the renal cortex. In this study, we have analysed the effect of low sodium feeding and AT1 receptor blockade on renal dopamine metabolism by monoamine oxidase. METHODS: Four groups of rats were studied: 1, normal salt diet (NS); 2, low salt diet (LS); 3, NS receiving Losartan (Los, specific AT1 receptor antagonist, 20 mg kg(-1) bwt day(-1), NS + Los); 4, LS receiving Los (LS + Los). RESULTS: Urinary dopamine excretion was lower in LS than in NS rats (543 +/- 32 vs. 680 +/- 34 ng day(-1) 100 g(-1) bwt, P < 0.05). When treated with Los, DOPAC excretion and urinary DOPAC/dopamine ratio fell significantly in the LS + Los group as compared with the LS group (1199 +/- 328 vs. 3081 +/- 681 ng day(-1) 100 g(-1) bwt and 1.90 +/- 0.5 vs. 5.7 +/- 1.2, respectively, both P < 0.02). Losartan increased hydroelectrolyte excretion in the LS group. No changes were found in the NS + Los group. Aromatic L-amino acid decarboxylase activity in cortex was similar in NS and LS rats. Instead, monoamine oxidase activity was higher in cortical homogenates from LS rats (in nmol mg tissue(-1) h(-1): NS 7.66 +/- 0.52; LS 9.82 +/- 0.59, P < 0.05) and this difference was abolished in LS + Los rats (7.34 +/- 0.49 nmol mg tissue(-1) h(-1), P < 0.01, vs. LS). CONCLUSIONS: We have concluded that low levels of dopamine in the urine of LS rats are because of an increase in the activity of renal monoamine oxidase and that angiotensin II mediates this increase through stimulation of AT1 receptors.

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This study assess the effects of glucocorticoids on dopamine excretion and evaluates the participation of renal dopamine in the effects of glucocorticoids on renal function and Na+ excretion. Dexamethasone (i.m.; 0.5 mg/kg) was administered to male Wistar rats on day 2 or on days 2 and 5. Daily urinary excretions of Na+, dihydroxyphenylalanine (DOPA), dopamine and dihydroxyphenylacetic acid were determined from day 1 to day 7. Renal function was evaluated 8 h after dexamethasone administration in a separate group. The first dose of dexamethasone increased about 100% diuresis and natriuresis, increased urinary DOPA and renal plasma flow, and did not affect urinary dopamine or the other parameters evaluated. These effects were not affected by previous administration of haloperidol. The second dexamethasone dose increased about 200% diuresis and natriuresis, increased urinary dopamine, DOPA, dihydroxyphenylacetic acid, Uosm x V and both glomerular filtration rate and renal plasma flow. Carbidopa administered before the second dexamethasone dose blunted both the diuretic and the natriuretic response whereas haloperidol abolished or blunted all the effects of the second dexamethasone dose. These results show that modifications in renal dopamine production produced by corticoids may contribute to the effects of these hormones on Na+ balance and diuresis and suggest that regardless the factor that promotes an increase in renal perfusion and glomerular filtration rate during long term administration of glucocorticoids, a dopaminergic mechanism is actively involved in the maintenance of these hemodynamic changes.

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El déficit atencional con hiperactividad es un síndrome que afecta de 5 a 10 por ciento de los niños en edad escolar y tiene severas consecuencias para el rendimiento intelectual, las relaciones intrafamiliares y el futuro de los niños afectados. Dado que el tratamiento con estimulantes es beneficioso en estos casos, con un diagnóstico positivo frente a patologías comórbidas como por ejemplo la depresión o la ansiedad, es muy importante. Por ello se determinó la excreción de noradrenalina a primeras horas de la mañana (8:00) y a media mañana (10:00) en niños controles y en portadores de déficit atencional con hiperactividad (DAH). Los datos obtenidos muestran que la dinámica de la noradrenalina se modifica en los niños con DAH. En los niños normales, la noradrenalina aumenta significativamente -hasta tres veces- en el correr de la mañana, adaptándose al ritmo de actividad normal. En los pacientes no se observa este aumento y, por el contrario, existe una tendencia a la disminución de la excreción de noradrenalina matinal. Los valores basales son similares en controles y pacientes. Se sugiere que existe una pérdida de la adaptación noradrenérgica y, por lo tanto, simpática, en el DAH. Estos cambios reflejarían la disfunción central -quizá a nivel de los ganglios basales- y junto a otras técnicas no invasivas -como la evaluación asistida por computadora- pueden ayudar al diagnóstico clínico del déficit atencional con hiperactividad

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