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PubMed1988

Effects of sodium restriction and energy reduction on erythrocyte sodium transport in obese hypertensive men.

Twelve moderately obese middle-aged male out-patients with untreated mild hypertension reduced their sodium intake by about 120 mmol/day during 4-6 weeks. The low sodium diet period was followed by a period of energy reduction as well as sodium restriction for 15 weeks. Mean body mass was then reduced by 7.5 +/- 1.0 kg. Intraerythrocyte sodium (IeNa), sodium influx (Na-influx) and sodium efflux rate constant (Na-efflux rate), were measured before intervention, during salt restriction and during salt and energy restriction. Plasma renin activity (PRA) and urinary excretion of aldosterone (U-Aldo) and noradrenaline (U-NA) were also determined during the three observation periods. During sodium restriction there was a significant increase in PRA and U-Aldo, but no change was seen in IeNa, Na-influx or Na-efflux rate constant. During sodium restriction there was a significant positive correlation between PRA and both Na-influx and Na-efflux rate constant. When energy reduction was combined with sodium restriction, PRA and U-NA both diminished significantly. Na-influx and Na-efflux rate also exhibited a significant decrease while IeNa did not change. Sodium restriction caused a significant fall in mean arterial blood pressure and a tendency to a further decrease was seen when energy intake was also reduced. No significant correlation could be found between the fall in blood pressure and changes in cellular sodium transport. These data indicate that the renin-angiotensin-aldosterone system and sympathetic activity influence the regulation of erythrocyte sodium turnover during sodium and energy restriction in obese hypertensive men.

Biological Transport↗
PubMed2003

Effect of sodium chloride on the release, absorption and safety of diclofenac sodium delivered by poloxamer gel.

Poloxamer solutions prepared with poloxamers and sodium chloride were previously reported to undergo a phase transition to bioadhesive gels at body temperature. For the development of a thermosensitive diclofenac sodium-loaded poloxamer gel, here we investigated the effect of sodium chloride on the release, safety and rectal absorption in rats of diclofenac sodium delivered by the poloxamer gels. P 188 delayed the release rates of diclofenac sodium from poloxamer gels. However, sodium chloride showed no significant effect on the release rates of diclofenac sodium from poloxamer gels. Release mechanism analysis showed the release of diclofenac sodium was proportional to the time. The initial plasma concentrations of diclofenac sodium in the rectal formulation [diclofenac sodium/poloxamer 407 (P 407)/poloxamer 188 (P 188)/sodium chloride (2.5/15/17/0.8%)] were significantly higher compared with those in semi-solid suppository. Furthermore, it gave significantly faster Tmax of diclofenac sodium than did semi-solid suppository, indicating that the diclofenac sodium from poloxamer gel could be absorbed faster than that from semi-solid one in rats. It did not cause any morphological damage to the rectal tissues. These results suggested that poloxamer gel with sodium chloride could be a more effective and safe rectal delivery system of diclofenac sodium.

Absorption↗
PubMed1990

Increased erythrocyte sodium-lithium countertransport activity in essential hypertension is due to an increased affinity for extracellular sodium.

1. Sodium-lithium countertransport activity in a standard assay, its sodium affinity constant and maximum velocity were measured in erythrocytes from normal subjects and from essential hypertensive patients with and without a family history of hypertension. 2. In normal subjects the sodium concentration used in the standard assay was similar to the sodium affinity constant so that the activity measured in this assay was less than the maximum velocity. 3. In patients with essential hypertension and a positive family history, 33% had a sodium-lithium countertransport activity greater than the upper limit of the normal control range (0.4 mmol of Li+ h-1 l-1 of cells). 4. The reason for the raised sodium-lithium countertransport activity was an increased sodium affinity (lower sodium affinity constant) at the outside ion-binding site. 5. Of the patients with essential hypertension and a positive family history but sodium-lithium countertransport activity within the normal range in the standard assay, 30% also had a low sodium affinity constant. 6. A low sodium affinity constant at the outside site of the sodium-lithium countertransporter may be a more specific indicator for a group of patients with inherited hypertension than the standard sodium-lithium countertransport activity assay.

Adult↗
PubMed1992

Inhibition profiles of sodium cromoglycate and nedocromil sodium on mediator release from mast cells of human skin, lung, tonsil, adenoid and intestine.

We have studied an aspect of the functional heterogeneity of human mast cells, namely responsiveness to the inhibitory effects of sodium cromoglycate and nedocromil sodium. The effects of these drugs were examined on the release of histamine and PGD2 from mast cells of human skin, lung, tonsils, adenoids and intestine. A high concentration, 1000 microM, of sodium cromoglycate was required to significantly inhibit histamine release from lung and tonsillar mast cells. Nedocromil sodium, 1000 microM, was more effective than sodium cromoglycate against histamine release from lung, tonsillar and adenoidal cells. Both compounds showed tachyphylaxis in lung and tonsillar mast cells but not in adenoidal and intestinal mast cells. In contrast, in intestinal mast cells, the effect of nedocromil sodium was weaker and more variable than sodium cromoglycate. Skin mast cells differed from mast cells of the other anatomical sites in being unresponsive to sodium cromoglycate and nedocromil sodium. Our results confirm that high concentrations of sodium cromoglycate and nedocromil sodium are required to achieve even modest inhibition of mediator release from human mast cells under in vitro conditions. Notwithstanding this, the results also indicate that differences exist among skin, lung, tonsillar, adenoidal and intestinal mast cells with respect to their sensitivity to sodium cromoglycate and nedocromil sodium, thus extending our knowledge of functional heterogeneity within the human mast cell populations.

Adenoids↗
PubMed2004

Effect of dietary sodium intake on blood lipids: results from the DASH-sodium trial.

We evaluated the effect on serum lipids of sodium intake in 2 diets. Participants were randomly assigned to a typical American control diet or the Dietary Approaches to Stop Hypertension (DASH) diet, each prepared with 3 levels of sodium (targeted at 50, 100, and 150 mmol/d per 2100 kcal). The DASH diet is increased in fruits, vegetables, and low-fat dairy products and is reduced in saturated and total fat. Within assigned diet, participants ate each sodium level for 30 days. The order of sodium intake was random. Participants were 390 adults, age 22 years or older, with blood pressure of 120 to 159 mm Hg systolic and 80 to 95 mm Hg diastolic. Serum lipids were measured at baseline and at the end of each sodium period. Within each diet, sodium intake did not significantly affect serum total cholesterol, LDL cholesterol, HDL cholesterol, or triglycerides. On the control diet, the ratio of total cholesterol-to-HDL cholesterol increased by 2% from 4.53 on higher sodium to 4.63 on lower sodium intake (P=0.04). On the DASH diet, sodium intake did not affect this ratio. There was no dose-response of sodium intake on serum lipids or the cholesterol ratio in either diet. At each sodium level, total cholesterol, LDL cholesterol, and HDL cholesterol were lower on the DASH diet versus the typical American diet. There were no significant interactions between the effects of sodium and the DASH diet on serum lipids. In conclusion, changes in dietary sodium intake over the range of 50 to 150 mmol/d did not affect blood lipid concentrations.

Adult↗
PubMed1978

Evidence for a splanchnic sodium input monitor regulating renal sodium excretion in man. Lack of dependence upon aldosterone.

Eight normal male subjects were placed on a constant 10 mEq sodium, 60 mEq potassium diet for 5 days. At 8:00 a.m. on the 5th day, the subjects were given a standard dose of 100 mEq of sodium orally or intravenously. Subjects receiving oral sodium also received 200ml of 5% dextrose in water intravenously, and those receiving intravenous sodium also received placebo capsules orally. Water intake and posture were controlled. The subjects then returned to a free diet for 1 month and subsequently were restudied by using the opposite route of sodium administration. The subjects given the oral sodium load excreted greater quantities of sodium in their urine than those repleted intravenously. The differential natriuresis was significant as early as 2 hours after sodium loading. Plasma aldosterone concentration was similar irrespective of the route of sodium administration. Six patients with primary adrenocortical insufficiency and documented hypoaldosteronism were studied with the same protocol after 5 days of 50 mEq sodium, 60 mEq potassium intake. They also had significantly greater natriuresis after oral than intravenous sodium administration. The data suggest the presence of a splanchnic input monitor for sodium which partially regulates renal sodium excretion and is not dependent upon a turn-off mechanism for aldosterone secretion.

Administration, Oral↗
PubMed1996

A comparative study of the clinical efficacy of nedocromil sodium and placebo. How does cromolyn sodium compare as an active control treatment?

Nedocromil sodium and cromolyn sodium are the only two currently available nonsteroid anti-inflammatory agents for treatment of asthma. Clinical differences between the two agents remain under continuous investigation with reports differentiating the two on the basis of atopy of the patient and reversibility of bronchoconstriction. This study investigated the efficacy of nedocromil sodium (4 mg, qid) for treatment of mild-to-moderate asthma in comparison to placebo using cromolyn sodium (2 mg, qid) as an active control treatment. Patients were primarily allergic asthmatics (with at least 15% reversibility) previously maintained on a regimen of regular bronchodilator therapy. During a 2-week run-in period, the patient's slow-release theophylline therapy was removed, and the patients were randomized to treatment after deterioration of asthma control (asthma symptom summary score of 3 for 7 of the 14 days). After 8 weeks of treatment, patients were returned to as occasion requires bronchodilator therapy, as per the 2-week baseline period. The results demonstrate that patients treated with nedocromil sodium showed statistically significant improvements during the primary time period (mean weeks 3 through 8) over placebo-treated patients as evidenced by all indexes of asthma symptoms, pulmonary function measures, and decreased bronchodilator reliance (p<0.05). Patients treated with cromolyn sodium demonstrated similar improvements over placebo-treated patients. Comparisons between nedocromil sodium and cromolyn sodium showed the two agents to be comparable in this group of primarily allergic patients with reversible disease. Between-group differences were noted for 3 of the 13 variables (nighttime asthma, FEV1, and forced expiratory flow rate between 25 % and 75% of the FVC) in favor of cromolyn sodium when the data were pooled during the primary time period. The number of patients missing 1 or more days from work/school/regular activity due to asthma was significantly fewer compared with placebo, and favoring nedocromil sodium over cromolyn sodium. No differences were observed among the three treatments for adverse events. This study demonstrated that in primarily allergic patients with reversible airways disease, nedocromil sodium and cromolyn sodium are both significantly more effective than placebo for treatment of mild-to-moderate asthma.

Activities of Daily Living↗
PubMed2001

Sodium balance-neutral sodium profiling does not improve dialysis tolerance.

BACKGROUND: Modern haemodialysis monitors offer computerised ultrafiltration and sodium concentration profiles which promise better dialysis tolerance. This presumption was tested in chronic haemodialysis patients. METHODS: Using Fresenius MC 4008S monitors a group of nine patients were dialysed with a given ultrafiltration profile comparing sessions with decreasing sodium concentration (145 to 133 mmol/L) to sessions with constant sodium concentration (138 mmol/L) in random order. The built-in blood volume monitor recorded changes in haematocrit and blood volume during each dialysis. The analyses included dialytic weight loss, interdialytic weight gain and adverse symptoms (hypotensive episodes and muscle cramps). RESULTS: 321 dialysis sessions, 160 with and 161 without sodium profile, were available for analysis. No significant differences could be detected regarding changes in haematocrit, blood volume and weight in relation to sodium profiling. No significant difference in the incidence of hypotension or muscle cramping was observed with 55 symptomatic dialyses of 160 with sodium profile, compared to 52 symptomatic dialyses of 161 without sodium profile. Interdialytic weight gain and consequent weight loss during dialysis was higher in symptomatic dialyses both with sodium profile or without sodium profile. The same was true of increase in haematocrit and decrease in blood volume, which were greater for symptomatic versus symptom-free dialyses irrespective of sodium profiling. CONCLUSIONS: Sodium balance-neutral sodium profiling failed to improve dialysis tolerance in a group of stable chronic haemodialysis patients. This may be explained by the fact that vascular refilling as deduced from changes in haematocrit was uninfluenced by sodium profiling.

Aged↗
PubMed1991

Sodium appetite in rats after prolonged dietary sodium deprivation: a sexually dimorphic phenomenon.

Little sodium appetite is observed when rats are deprived of dietary sodium for several days, presumably because aldosterone secretion minimizes renal sodium losses. However, the present studies indicate that when sodium deprivation is extended to 8 days, a spontaneous sodium appetite results that far exceeds urinary sodium losses during the deprivation period; indeed, adult male rats drank as much 0.5 M NaCl solution as rats ever have been reported to drink rapidly. In contrast, female rats drank much less saline after 8 days of sodium deprivation. Because of this sexual dimorphism in sodium appetite, we also studied NaCl intake in gonadectomized rats after 8 days of sodium deprivation. Both male and female gonadectomized rats drank comparable amounts of saline as intact male rats, but they consumed much less when treated with physiological amounts of estrogen during the sodium-deprivation period. These results indicate that a robust appetite for NaCl can be produced in rats by prolonged sodium deprivation and that estrogen can blunt the induced sodium appetite.

Administration, Oral↗
PubMed1994

A serial study of erythrocyte sodium pump kinetics and sodium content in the puerperium.

OBJECTIVE: Our purpose was to describe the alterations in erythrocyte sodium pump kinetics and sodium content occurring during the puerperium. STUDY DESIGN: Twelve healthy primigravid women were studied serially from late pregnancy until 20 weeks after delivery. Erythrocyte sodium pump rate constant, maximum velocity, and sodium affinity were calculated from the ouabain-sensitive sodium flux measured in whole blood and in erythrocytes in which sodium content had been altered with the ionophore nystatin. The Student t test was used to compare the regression coefficients of the values plotted against log time for specific periods. RESULTS: The sodium pump rate constant, maximum velocity, and sodium affinity were lower 20 weeks after delivery than in late pregnancy (0.339 +/- 0.018 vs 0.399 +/- 0.016/hr, 7.02 +/- 0.08 vs 9.98 +/- 0.078 mmol/kg/hr, 2.65 +/- 0.21 vs 3.16 +/- 0.20 mmol/kg). The decrease in the rate constant commenced after 4 days of the puerperium, whereas the decrease in maximum velocity and Michaelis-Menten constant did not commence until after 2 weeks. Erythrocyte sodium content was greater 20 weeks after delivery than in late pregnancy (4.71 +/- 0.20 vs 4.14 +/- 0.15 mmol/kg cells) and the increase was gradual over the time studied. CONCLUSIONS: After delivery the rate constant of the sodium pump measured in plasma and the erythrocyte sodium content changed before any significant alteration in the maximum velocity of the pump. The return of sodium pump function to the nonpregnant state continues beyond 6 weeks after delivery.

Erythrocytes↗
PubMed1982

Effects of chronic sodium depletion on renal tubular sodium and water reabsorption in man.

In order to assess the effects of sodium depletion on tubular Na and H2O transport in man, renal clearance studies were performed under control conditions and after sodium depletion in 7 normal subjects. The control diet contained 250 mEq of Na daily. Sodium depletion was induced by placing subjects on a 20-mEq/day na diet and administering furosemide (40 mg) dialy for 3 days. Balance studies revealed that the subjects were in Na balance under control conditions, and that after sodium depletion had been established they were in a sodium-retaining state. Subjects were studied under both conditions, after H2O hydration and during a subsequent hypotonic mannitol infusion. After H2O hydration the minimal urinary osmolality averaged 61 and 67 mosm/kg in the sodium depletion and control states, respectively. Sodium depletion was associated with a significant reduction in C inulin, sodium clearance (CNa), urine flow (V), fractional urine flow (V/GFR), free water (CH2O), and fractional free water clearance (CH2O/GFR). During hypotonic mannitol infusion indices of absolute and fractional delivery of Na from the proximal tubule (CH2O + CNa; CH2O/GFR + CNa/GFR) were consistently reduced after sodium depletion and rose more slowly as absolute and fractional distal sodium chloride supply (CH2O + CNa; CH2O/GFR + CNa/GFR) were increased. These data are consistent with the view that modest sodium depletion in man provokes an increase in fractional sodium chloride reabsorption in both the proximal and distal tubules.

Absorption↗
PubMed1987

Effect of sodium intake on blood pressure, serum levels and renal excretion of sodium and potassium in normotensives with and without familial predisposition to hypertension.

1. Seventeen normal volunteers aged 19 to 22 were randomly subjected, in a trial of crossover design, to three distinct regimens of sodium chloride intake: high (16 to 20 g), normal (8 to 12 g) and low (0.5 to 1 g). Each regimen lasted nine days, with determination of blood pressure and heart rate (in the supine position and after sudden rising), body weight, and urinary output of creatinine, sodium and potassium on the third, sixth and ninth days. In addition, plasma levels of creatinine, sodium and potassium were determined on the ninth day so that sodium and potassium clearance and fractional excretion could be calculated. 2. Eleven of the volunteers had a family history of hypertension. Compared to the six without such a history, these subjects showed: 1) higher supine systolic blood pressure on the third day of sodium overload (124.7 +/- 3.0 vs 112.3 +/- 2.9 mmHg, P less than 0.02); 2) higher supine diastolic blood pressure on the third day of sodium overload (76.5 +/- 2.8 vs 64.5 +/- 4.3 mmHg; P less than 0.05); 3) higher supine diastolic blood pressure on the sixth day of sodium overload (73.7 +/- 2.3 vs 63.8 +/- 3.2 mmHg, P less than 0.05); 4) lower supine heart rate on the ninth day of sodium overload (61.0 +/- 3.1 vs 72.7 +/- 4.6, P less than 0.05), and 5) lower plasma potassium on the ninth day of sodium overload (4.10 +/- 0.05 vs 4.28 +/- 0.06 mEq/l, P less than 0.05). 3. These results suggest that normal individuals whose familial history places them at risk for the development of hypertension differ from those not at risk during their adaptation to sodium load by suffering a transient elevation of blood pressure within a few days of the increase in load. The low levels of plasma potassium observed in these volunteers after a period of sodium load may be due to the operation of different renal mechanisms of sodium excretion in this group, leading to increased kaliuresis, and may explain the high vascular reactivity of such individuals.

Adult↗
PubMed1985

Hemodynamics and sodium balance in conscious sodium-depleted rats.

The objective of this paper was to study the hemodynamics (mean arterial pressure, cardiac output, total peripheral resistance, stroke volume and heart rate) of conscious rats submitted to 6 days of sodium depletion. Sodium balance of sodium-depleted rats on a low-sodium diet (0.1 mEq/day) associated with furosemide (10 mg/kg, ip on the first and fifth day) for 6 days indicated that the animals were studied under a negative sodium balance on the sixth day. The overactivity of the renin-angiotensin system in sodium-depleted rats was demonstrated by the fall in mean arterial pressure (15 +/- 2 vs 0.5 +/- 1 mmHg in sodium-depleted and control rats, respectively), after blocking the converting enzyme with BPP9a (SQ 20881) and also by evaluating plasma renin activity (10 +/- 8 vs 3.0 +/- 0.6 ng AI ml-1 h-1 in sodium-depleted and control rats, respectively). Thermodilution measurements showed that the cardiac output of sodium-depleted animals was reduced by 35% (29 +/- 2 vs 45 +/- 4 ml min-1 100 g-1 for sodium-depleted and control rats, respectively), with partial compensation by a 37% increase in total peripheral resistance (3.7 +/- 0.3 vs 2.7 +/- 0.2 PRU for sodium-depleted and control rats, respectively), resulting in an 11% decrease in mean arterial pressure (104 +/- 5 vs 117 +/- 3 mmHg for sodium-depleted and control rats, respectively).

Animals↗
PubMed1979

Cyanide intoxication in sheep: enhancement of efficacy of sodium nitrite, sodium thiosulfate, and cobaltous chloride.

For treatment of cyanide intoxication of ruminants, the present recommended doses of sodium nitrite (5 mg/kg of body weight) and sodium thiosulfate (25 to 50 mg/kg) are smaller than those recommended for other animals; the decrease is partially attributed to the greater susceptibility of ruminants to the toxic effects of sodium nitrite. Based on the high tissue concentration and activity rate of rhodanese in ruminants, sulfur donors such as sodium thiosulfate could be utilized more efficaciously. Doses of sodium nitrite and sodium thiosulfate (up to 22 and 660 mg/kg, respectively) were evaluated in the present studies. Adjustment of the antidotal combination provided almost three times the protection afforded by the previously recommended doses. Moreover, under the conditions tested, the newly adjusted dose levels of sodium thiosulfate alone were more effective than the previously used antidotal combination of sodium nitrite and sodium thiosulfate and this protective effect was enhanced by cobaltous chloride (10.6 mg/kg) or sodium nitrite. The present recommended therapeutic approach to cyanide intoxication in sheep should be based primarily on administration of a much higher dose of sodium thiosulfate in combination with sodium nitrite or cobaltous chloride (or both).

Animals↗
PubMed1995

Natriuretic response to acute sodium chloride or sodium bicarbonate infusions in humans.

We compared the natriuretic responses to acute sodium chloride or sodium bicarbonate loading. 2.25 mEq/kg of sodium as sodium chloride, or sodium bicarbonate was infused intravenously in 1 h. Sodium chloride infusion resulted in a gradual increase in urinary sodium excretion (UNaV) for 4 h after starting the infusion, while sodium bicarbonate infusion caused a transient increase in UNaV for the first 2 h followed by a decrease. The amount of sodium excreted over 4 h in the sodium chloride and sodium bicarbonate groups were 20.7 +/- 4.7 and 34.8 +/- 2.3% of the sodium loaded, respectively (p < 0.05). This difference could not be ascribed to divergent responses in glomerular filtration rate, aldosterone, atrial natriuretic peptide, or serum albumin concentration. The difference in UNaV might be caused by the differences in renal tubular handling of chloride and bicarbonate.

Adult↗