996 resultados para SODIUM EXCRETION


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"Introdução: O pão tem sido apontado como um alimento relevante no aporte total de sódio de algumas populações. Em 2009 em Portugal, o consumo anual de pão per capita foi cerca de 70 kg. As atuais recomendações de aporte de sal são quase sempre excedidas, sendo este facto mais grave em indivíduos idosos e hipertensos. Objetivo: Avaliar a contribuição do consumo de pão no aporte total de sódio diário em idosos institucionalizados e avaliar junto da instituição em pesquisa, o potencial efeito e o cumprimento da lei n.º 75/2009 com entrada em vigor a 12 de Agosto de 2010."

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BACKGROUND: Salt reduction is a public health priority but there are few studies testing the efficacy of plausible salt reduction programs.

METHODS: A multi-faceted, community-based salt reduction program using the Communication for Behavioral Impact framework was implemented in Lithgow, Australia. Single 24-h urine samples were obtained from 419 individuals at baseline (2011) and from 572 at follow-up (2014). Information about knowledge and behaviors relating to salt was also collected.

RESULTS: Survey participants were on average 56 years old and 58 % female. Mean salt intake estimated from 24-h urine samples fell from 8.8 g/day (SD = 3.6 g/day) in 2011 to 8.0 (3.6) g/day in 2014 (-0.80, 95 % confidence interval -1.2 to -0.3;p < 0.001). There were significant increases in the proportion of participants that knew the recommended upper limit of salt intake (18 % vs. 29 %; p < 0.001), knew the importance of salt reduction (64 % vs. 78 %; p < 0.001) and reported changing their behaviors to reduce their salt intake by using spices (5 % vs. 28 %; p < 0.001) and avoiding eating out (21 % vs. 34 %; p < 0.001). However, the proportions that checked food labels (30 % vs. 25 %; p = 0.02) fell, as did the numbers avoiding processed foods (44 % vs. 35 %; p = 0.006). Twenty-six percent reported using salt substitute at the end of the intervention period and 90 % had heard about the program. Findings were robust to multivariable adjustment.

CONCLUSIONS: Implementation of this multi-faceted community-based program was associated with a ~10 % reduction in salt consumption in an Australian regional town. These findings highlight the potential of well-designed health promotion programs to compliment other population-based strategies to bring about much-needed reductions in salt consumption.

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Twenty-four-hour urine collection is the recommended method for estimating sodium intake. To investigate the strengths and limitations of methods used to assess completion of 24-hour urine collection, the authors systematically reviewed the literature on the accuracy and usefulness of methods vs para-aminobenzoic acid (PABA) recovery (referent). The percentage of incomplete collections, based on PABA, was 6% to 47% (n=8 studies). The sensitivity and specificity for identifying incomplete collection using creatinine criteria (n=4 studies) was 6% to 63% and 57% to 99.7%, respectively. The most sensitive method for removing incomplete collections was a creatinine index <0.7. In pooled analysis (≥2 studies), mean urine creatinine excretion and volume were higher among participants with complete collection (P<.05); whereas, self-reported collection time did not differ by completion status. Compared with participants with incomplete collection, mean 24-hour sodium excretion was 19.6 mmol higher (n=1781 specimens, 5 studies) in patients with complete collection. Sodium excretion may be underestimated by inclusion of incomplete 24-hour urine collections. None of the current approaches reliably assess completion of 24-hour urine collection.

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The circumventricular structures and the lateral hypothalamus (LH) have been shown to be important for the central action of angiotensin II (ANGII) on water and electrolyte regulation. Several anatomical findings have demonstrated neural connection between circumventricular structures and the LH, the present experiments were conducted to investigate the role of the alpha-adrenergic antagonists and agonistic injected into the LH on the water intake, sodium and potassium excretion elicited by injections of ANGII into the lateral ventricle (LV), the water intake was measured every 30 min over a period of 120 min. The sodium, potassium and urinary volume were measured over a period of 120 min in water-loaded rats. The injection of ANGII into the LV increased the water intake, which was reduced by previous injection of clonidine (an alpha-2-adrenergic agonist) into the LH. The injection of yohimbine (an alpha-2-adrenergic antagonist) and prazosin (an alpha-l-adrenergic antagonist) into the LH, which was done before injecting ANGII into the LV, also reduced the water intake induced by ANGII. The injection of ANGII into the LV reduced the sodium, potassium and urinary volume. Previous treatment with clonidine attenuated the action of ANGII in reducing the sodium, potassium and urinary volume, whereas previous treatment with yohimbine attenuated the effects of ANGII but with less intensity than that caused by clonidine. Previous treatment with prazosin increased the inhibitory effects of ANGII in those parameters. The injection of yohimbine and prazosin, which was done before the injection of clonidine, attenuated the effect of clonidine on the ANGII mechanism. The results of this study led us to postulate that when alpha-2-adrenergic receptors are blocked, the clonidine may act on the imidazoline receptors to produce its effects on the ANGII mechanism. We may also conclude that the LH is involved with circumventricular structures, which present excitatory and inhibitory mechanisms. Such mechanisms are responsible for regulating the renal excretion of sodium, potassium and water, (C) 2000 Elsevier B.V.

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The effects of sodium and potassium excretion after intrahypothalamic administration of two α-adrenoceptor agonists and the effect of α-adrenoceptor antagonists were studied in groups of rats. Prazosin was equally effective at blocking the natriuretic and kaliuretic responses to the α1-adrenoceptor agonist phenylephrine and the mixed α1/α2-adrenoceptor agonist noradrenaline, while yohimbine which acts preferentially on α2-adrenoceptors was effective in potentiating these responses. These results suggest the presence of two types of α-adrenoceptors for the modulation of ventromedial hypothalamic pathways that interfere with the regulation of the two cations: stimulation of α1-adrenoceptors facilitates, while stimulation of α2-adrenoceptors inhibits the excretion of the ions.

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Previous studies have suggested that oral or intravenous glucose enhances salt and water retention following a saline load. To test this, we studied the effects of an oral glucose load on urinary sodium and water excretion and serum biochemistry in response to a 2l intravenous infusion of 0.9% saline in normal subjects.

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The aim of this study was to assess the association between parent and child sodium (Na) and potassium (K) intake as assessed by 24-h urinary excretion (24hUE). Primary school children and their parent(s) provided one 24-h urine sample and information on cooking and children's discretionary salt use. Valid urine samples were provided by 108 mothers (mean age 41.8 (5.1) (SD) years, Na 120 (45) mmol/day) (7.0 g/day salt equivalent) and 40 fathers (44.4 (4.9) years, Na 152 (49) mmol/day (8.9 g/day salt), and 168 offspring (51.8% male, age 9.1 (2.0) years, Na 101 (47) mmol/day (5.9 g/day salt). When adjusted for parental age, child age and gender a 17 mmol/day Na (1 g/day salt) increase in mother's 24hUE was associated with a 3.4 mmol/day Na (0.2 g/day salt) increase in child's salt 24hUE (p = 0.04) with no association observed between father and child. Sixty-seven percent of parents added salt during cooking and 37% of children added salt at the table. Children who reported adding table salt had higher urinary excretion than those who did not (p = 0.01). The association between mother and child Na intake may relate to the consumption of similar foods and highlights the importance of the home environment in influencing total dietary sodium intake.

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A cohort of 161 underground miners who had been highly exposed to dinitrotoluene (DNT) in the copper-mining industry of the former German Democratic Republic was reinvestigated for signs of subclinical renal damage. The study included a screening of urinary proteins excreted by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), and quantitations of the specific urinary proteins α 1-microglobulin and glutathione-S-transferase α (GST α) as biomarkers for damage of the proximal tubule and glutathione-S-transferase π (GST π) for damage of the distal tubule. The exposures were categorized semiquantitatively (low, medium, high, and very high), according to the type and duration of professional contact with DNT. A straight dose-dependence of pathological protein excretion patterns with the semiquantitative ranking of DNT exposure was seen. Most of the previously reported cancer cases of the urinary tract, especially those in the higher exposed groups, were confined to pathological urinary protein excretion patterns. The damage from DNT was directed toward the tubular system. In many cases, the appearance of Tamm-Horsfall protein, a 105-kD protein marker, was noted. Data on the biomarkers α 1-microglobulin, GST α, and GST π consistently demonstrated a dose-dependent increase in tubular damage, which confirmed the results of screening by SDS-PAGE and clearly indicated a nephrotoxic effect of DNT under the given conditions of exposure. Within the cluster of cancer patients observed among the DNT-exposed workers, only in exceptional cases were normal biomarker excretions found.

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1. Since salt depletion stimulates the renal prostaglandin system to maintain renal function, the effects of indomethacin and ibuprofen upon renal haemodynamics, electrolyte excretion and renin release were examined in eight healthy male volunteers on a salt restricted diet, before and after frusemide administration. 2. Neither indomethacin (50 mg) nor ibuprofen (400 mg and 800 mg) affected renal blood flow, glomerular filtration rate or electrolyte excretion before frusemide. 3. Renal blood flow and glomerular filtration rate were significantly increased in the first 20 min after frusemide. These changes were significantly attenuated by indomethacin compared with placebo and ibuprofen 400 mg. Frusemide-induced diuresis but not natriuresis was inhibited by all treatments. 4. Both nonsteroidal agents inhibited equally the rise in renin activity seen after frusemide. 5. In this group of healthy volunteers on a salt restricted diet, ibuprofen and indomethacin had no detrimental effects on renal function in the absence of frusemide. The changes in renal haemodynamics due to frusemide were suppressed more by indomethacin than by ibuprofen, probably reflecting the more potent nature of indomethacin as an inhibitor of prostaglandin synthesis.

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1. This study has compared the effects of ibuprofen and indomethacin upon renal haemodynamics, electrolyte excretion and renin release in the presence and absence of frusemide under sodium replete conditions in eight healthy volunteers. 2. Neither ibuprofen (400 mg and 800 mg) nor indomethacin (50 mg) affected renal blood flow, glomerular filtration rate or electrolyte excretion in the basal state. 3. Frusemide had no effect on renal blood flow, but significantly increased glomerular filtration rate. This latter change was suppressed significantly only by ibuprofen 400 mg. Frusemide-induced diuresis was inhibited by all treatments, while natriuresis following frusemide was inhibited by indomethacin only. 4. Significant increments in plasma renin activity, which were suppressed by all treatments, were observed after frusemide. The degree of inhibition of the renin responses was significantly greater in the presence of indomethacin than with either dose of ibuprofen. 5. In a sodium replete setting in healthy volunteers, indomethacin and ibuprofen had no detrimental effects on basal renal function. In the presence of frusemide, indomethacin had more anti-natriuretic and renin-suppressing effect than ibuprofen. There was no evidence for a dose-related effect of ibuprofen.

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The metabolic and respiratory effects of intravenous 0.5 M sodium acetate (at a rate of 2.5 mmol/min during 120 min) were studied in nine normal human subjects. O2 consumption (VO2) and CO2 production (VCO2) were measured continuously by open-circuit indirect calorimetry. VO2 increased from 251 +/- 9 to 281 +/- 9 ml/min (P < 0.001), energy expenditure increased from 4.95 +/- 0.17 kJ/min baseline to 5.58 +/- 0.16 kJ/min (P < 0.001), and VCO2 decreased nonsignificantly (211 +/- 7 ml/min vs. 202 +/- 7 ml/min, NS). The extrapulmonary CO2 loss (i.e., bicarbonate generation and excretion) was estimated at 48 +/- 5 ml/min. This observation is consistent with 1 mol of bicarbonate generated from 1 mol of acetate metabolized. Alveolar ventilation decreased from 3.5 +/- 0.2 l/min basal to 3.1 +/- 0.2 l/min (P < 0.001). The minute ventilation (VE) to VO2 ratio decreased from 22.9 +/- 1.3 to 17.6 +/- 0.9 l/l (P < 0.005), arterial PO2 decreased from 93.2 +/- 1.9 to 78.7 +/- 1.6 mmHg (P < 0.0001), arterial PCO2 increased from 39.2 +/- 0.7 to 42.1 +/- 1.1 mmHg (P < 0.0001), pH from 7.40 +/- 0.005 to 7.50 +/- 0.007 (P < 0.005), and arterial bicarbonate concentration from 24.2 +/- 0.7 to 32.9 +/- 1.1 (P < 0.0001). These observations indicate that sodium acetate infusion results in substantial extrapulmonary CO2 loss, which leads to a relative decrease of total and alveolar ventilation.