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At least 19 recordsLinked to original sources
PubMed1967

Facftors affecting the relative magnitudes of the sodium:potassium and sodium:sodium exchanges catalysed by the sodium pump.

1. The effects of external potassium on sodium: potassium exchange and sodium: sodium exchange in human red cells have been estimated from measurements of ouabain-sensitive potassium influx and ouabain-sensitive sodium influx in media containing different concentrations of potassium.2. As the external potassium concentration is increased from zero to 5 mM, sodium:sodium exchange-as judged by ouabain-sensitive sodium influx-is progressively suppressed, and sodium:potassium exchange-as judged by ouabain-sensitive potassium influx-is progressively increased. Both exchanges are half-maximal between 1 and 2 mM-K, and at 5 mM-K sodium: sodium exchange becomes very small as sodium: potassium exchange approaches a maximum.3. Experiments have been carried out, mainly on resealed ghosts, to determine what factors affect the magnitude of the sodium:sodium exchange in potassium-free solutions.4. Sodium:sodium exchange does not occur in the absence of adenosine triphosphate (ATP).5. Ghosts containing high concentrations of sodium, no potassium and high concentrations of ATP show no ouabain-sensitive loss of sodium into potassium-free solutions. The ability to carry out sodium:sodium exchange can be restored by replacing most of the internal sodium with potassium or by preparing the cells so that they contain much more orthophosphate (P(i)) than ATP.6. Ghosts containing sodium in low concentration, potassium in high concentration and with a low [ATP]/([ADP].[P(i)]) ratio show a greater ouabain-sensitive loss of sodium into potassium-free media than into media containing potassium; i.e. external potassium reduces ouabain-sensitive sodium efflux.7. The effect of P(i) is not the result of competitive inhibition of the transport ATPase since P(i) at the concentrations used does not inhibit ATPase activity in fragmented ghosts.

Adenine Nucleotides↗
PubMed1981

The magnesium dependence of sodium-pump-mediated sodium-potassium and sodium-sodium exchange in intact human red cells.

1. The magnesium content of human red blood cells was controlled by varying the magnesium concentration in the medium in the presence of the ionophore A23187. The new magnesium levels attained were very stable, which allowed the magnesium dependence of the sodium pump to be investigated.2. The effects of magnesium were shown to occur at the inner surface of the red cell membrane for the range of magnesium concentrations tested (10(-7) to 6 x 10(-3)m).3. At intracellular ionized magnesium concentrations below 0.8 mm the activation of ouabain-sensitive sodium-potassium exchange by internal ionized magnesium could be resolved into two or three components: (a) a small component, about 5% of the maximum flux, which is apparently independent of the ionized magnesium concentration below 2 mum, (b) a saturating component with a K((1/2)) of between 30 and 45 mum, and possibly (c) a component which increases linearly with ionized magnesium concentration and which only becomes apparent at concentrations above 0.1 mm.4. At intracellular ionized magnesium concentrations below 0.8 mm, activation of ouabain-sensitive sodium-sodium exchange by internal ionized magnesium could be resolved into two components: (a) a small component, about 6% of the maximal flux, which is apparently independent of the ionized magnesium concentration below 2 mum, and (b) a saturating component with a K((1/2)) of about 9 mum. At ionized magnesium concentrations between about 0.2 and 0.8 mm the rate of sodium-sodium exchange remained constant at the maximal level.5. The intracellular concentration of ATP decreased and the ADP concentration increased as the magnesium content of the cells was reduced from the normal level. A small increase in ATP and a small decrease in ADP was seen when the magnesium content was increased above the normal level. The variation in the ATP: ADP ratio from 2.5 at very low magnesium levels to about 6 at normal magnesium levels can account, at least in part, for the different K((1/2)) values of sodium-potassium and sodium-sodium exchange.6. When the concentration of ionized magnesium was increased above about 0.8 mm both sodium-potassium and sodium-sodium exchange were inhibited. Sodium-sodium exchange was more strongly inhibited than sodium-potassium exchange.7. The possible sites of action of magnesium in the sodium pump cycle are discussed.

Adenosine Diphosphate↗
PubMed1985

[Transmembrane effects in the sodium pump system. II. The ratio of the sodium efflux to the sodium concentration in frog muscle in media with various sodium substitutes].

The dependence of sodium efflux on the internal sodium concentration on sodium-free magnesium, Tris, coline and lithium media was investigated on frog striated muscle. In all the sodium-substituted media, the efflux concentration curve was found to be dependent on the external rubidium concentration, being S-shaped at the saturating external rubidium (potassium) concentration and becoming close to linear at the low external rubidium concentration (0.5-1.0 microM). The maximal sodium efflux at saturating levels of internal sodium concentrations remains unchanged with various sodium substitutes in the medium, whereas the affinity constant of internal sodium sites is dependent on the external cations.

Animals↗
PubMed2003

Final report on the safety assessment of sodium sulfite, potassium sulfite, ammonium sulfite, sodium bisulfite, ammonium bisulfite, sodium metabisulfite and potassium metabisulfite.

Sodium Sulfite, Ammonium Sulfite, Sodium Bisulfite, Potassium Bisulfite, Ammonium Bisulfite, Sodium Metabisulfite, and Potassium Metabisulfite are inorganic salts that function as reducing agents in cosmetic formulations. All except Sodium Metabisulfite also function as hair-waving/straightening agents. In addition, Sodium Sulfite, Potassium Sulfite, Sodium Bisulfite, and Sodium Metabisulfite function as antioxidants. Although Ammonium Sulfite is not in current use, the others are widely used in hair care products. Sulfites that enter mammals via ingestion, inhalation, or injection are metabolized by sulfite oxidase to sulfate. In oral-dose animal toxicity studies, hyperplastic changes in the gastric mucosa were the most common findings at high doses. Ammonium Sulfite aerosol had an acute LC(50) of >400 mg/m(3) in guinea pigs. A single exposure to low concentrations of a Sodium Sulfite fine aerosol produced dose-related changes in the lung capacity parameters of guinea pigs. A 3-day exposure of rats to a Sodium Sulfite fine aerosol produced mild pulmonary edema and irritation of the tracheal epithelium. Severe epithelial changes were observed in dogs exposed for 290 days to 1 mg/m(3) of a Sodium Metabisulfite fine aerosol. These fine aerosols contained fine respirable particle sizes that are not found in cosmetic aerosols or pump sprays. None of the cosmetic product types, however, in which these ingredients are used are aerosolized. Sodium Bisulfite (tested at 38%) and Sodium Metabisulfite (undiluted) were not irritants to rabbits following occlusive exposures. Sodium Metabisulfite (tested at 50%) was irritating to guinea pigs following repeated exposure. In rats, Sodium Sulfite heptahydrate at large doses (up to 3.3 g/kg) produced fetal toxicity but not teratogenicity. Sodium Bisulfite, Sodium Metabisulfite, and Potassium Metabisulfite were not teratogenic for mice, rats, hamsters, or rabbits at doses up to 160 mg/kg. Generally, Sodium Sulfite, Sodium Metabisulfite, and Potassium Metabisulfite were negative in mutagenicity studies. Sodium Bisulfite produced both positive and negative results. Clinical oral and ocular-exposure studies reported no adverse effects. Sodium Sulfite was not irritating or sensitizing in clinical tests. These ingredients, however, may produce positive reactions in dermatologic patients under patch test. In evaluating the positive genotoxicity data found with Sodium Bisulfite, the equilibrium chemistry of sulfurous acid, sulfur dioxide, bisulfite, sulfite, and metabisulfite was considered. This information, however, suggests that some bisulfite may have been present in genotoxicity tests involving the other ingredients and vice versa. On that basis, the genotoxicity data did not give a clear, consistent picture. In cosmetics, however, the bisulfite form is used at very low concentrations (0.03% to 0.7%) in most products except wave sets. In wave sets, the pH ranges from 8 to 9 where the sulfite form would predominate. Skin penetration would be low due to the highly charged nature of these particles and any sulfite that did penetrate would be converted to sulfate by the enzyme sulfate oxidase. As used in cosmetics, therefore, these ingredients would not present a genotoxicity risk. The Cosmetic Ingredient Review Expert Panel concluded that Sodium Sulfite, Potassium Sulfite, Ammonium Sulfite, Sodium Bisulfite, Ammonium Bisulfite, Sodium Metabisulfite, and Potassium Metabisulfite are safe as used in cosmetic formulations.

Animals↗
PubMed1979

Sodium excretion in man, and adaptation to a low-sodium diet: effect of intravenous sodium chloride.

1. The aim of this study was to test whether a postulated gastrointestinal or portal monitor of sodium intake plays any part in adjusting renal sodium excretion when dietary sodium is reduced. 2. Normal male subjects were given 50 mmol of sodium chloride intravenously three times daily for 3 days to replace or to supplement a constant oral intake of sodium chloride. 3. When oral sodium chloride was replaced with intravenous sodium chloride, renal sodium excretion remained constant. 4. When oral sodium chloride was kept constant, sodium administered as intravenous sodium chloride was promptly excreted in three out of four subjects. There was a delay in the increase in sodium excretion in the fourth subject. 5. Infusions containing 50 mmol of sodium chloride in 50 ml given intravenously over 22 min produced a rise in plasma sodium concentration and a fall in concentration of total plasma solids. 6. These results provide no evidence for a gastrointestinal or portal monitor of sodium intake, but do not disprove the existence of such a monitor.

Adult↗
PubMed1982

Blood pressure and sodium excretion in the sinoaortic denervated rat during chronic high and low sodium intake and acute sodium loading.

We studied the effects of dietary sodium on the magnitude of hypertension in sinoaortic denervated (SAD) rats. Groups of SAD rats and sham operated (SO) controls drank tap water and received chows with different amounts of sodium: low (0.08%), regular (0.4%), high (3%) or very high (7%) sodium; other groups, some after unilateral nephrectomy, received regular chow and 1% saline to drink. These various sodium regimens were started before operations and were continued for at least 12 weeks after SAD and SO. Weekly systolic tail-cuff pressures of SAD rats were significantly higher throughout the 12 week postoperative period than those of SO rats regardless of sodium regimen (p less than 0.05 to less than 0.01). Analysis of variance indicated no significant differences between pressures of SAD rats on regular or low sodium chows and those receiving any of the high sodium regimens. When SAD rats were switched from regular to high sodium diets no significant change was induced in systolic pressures. We then examined renal sodium excretion in response to oral sodium loading or to intravenous saline infusion in groups of SAD and SO rats. Both types of studies revealed that SAD rats excreted the extra sodium significantly faster than SO rats. We conclude that hypertension induced by SAD is not dependent on the amount of sodium in the diet and that the magnitude of hypertension is not increased by chronic high sodium intake. The rapid excretion of sodium suggests SAD rats have an enhanced sensitivity to activation and/or to effects of neural and/or humoral factors affecting renal sodium excretion.

Animals↗
PubMed2002

Time-averaged concentration of dialysate sodium relates with sodium load and interdialytic weight gain during sodium-profiling hemodialysis.

BACKGROUND: Factors determining sodium level during sodium-profiling hemodialysis rarely have been studied. We hypothesized that the time-averaged concentration of dialysate sodium (TAC(Na)) is related to intradialytic sodium load and interdialytic complications. METHODS: Eleven patients underwent 6-week periods of (1) conventional hemodialysis with a dialysate sodium concentration of 138 mmol/L (TAC(138)) and (2) sodium-profiling hemodialysis with a dialysate sodium concentration of 150 to 138 mmol/L (TAC(Na), 140 mmol/L [TAC(140)]) and (3) 155 to 130 mmol/L (TAC(Na), 147 mmol/L [TAC(147)]). Serum sodium level, weight gain, 24-hour blood pressure, and intradialytic and interdialytic discomfort were compared. RESULTS: Serum sodium levels increased during the TAC(140) and TAC(147) periods (P < 0.05 compared with predialysis serum sodium). Intradialytic change in sodium level correlated positively with TAC(Na) (r = 0.945; P < 0.001). Regression analysis indicates that positive sodium load occurred with TAC(Na) more than 137.8 mmol/L. Interdialytic weight gain increased in proportion to TAC(Na) (P < 0.05 compared with each other period), with a positive correlation (r = 0.823; P < 0.001). TAC(Na) causing interdialytic weight gain less than 3 kg was estimated to be less than 143.5 mmol/L. Intradialytic hypotension decreased, but interdialytic discomforts increased during the TAC(147) period (P < 0.05 compared with TAC(138) and TAC(140)). Mean 24-hour blood pressures and pressure loads increased during the TAC(147) period (P < 0.05 compared with TAC(138) and TAC(140)). Mean diastolic blood pressure correlated positively with TAC(Na) (r = 0.354; P < 0.05). CONCLUSION: TAC(Na) is a factor determining sodium load and interdialytic complications during sodium-profiling hemodialysis. Defining the optimal TAC(Na) for individual centers based on their protocols will be helpful to avoid sodium load and excessive weight gain.

Blood Pressure↗
PubMed1989

Sodium restriction and blood pressure in hypertensive type II diabetics: randomised blind controlled and crossover studies of moderate sodium restriction and sodium supplementation.

OBJECTIVE: To determine the effect of moderate dietary sodium restriction on the hypertension of non-insulin-dependent (type II) diabetes. DESIGN: Randomised parallel controlled study of moderate sodium restriction for three months compared with usual diabetic diet, followed by randomised double blind crossover trial of sustained release preparation of sodium for one month versus placebo for one month in patients continuing with sodium restriction. SETTING: Patients attending diabetic outpatient clinic of city hospital. PATIENTS: Thirty four patients with established type II diabetes complicated by mild hypertension (systolic blood pressure greater than 160 mm Hg or diastolic pressure greater than 95 mm Hg on three consecutive occasions). Patients already taking antihypertensive agents (but not diuretics) not barred from study provided that criteria for mild hypertension still met. Conditions precluding patients from study were diabetic or hypertensive nephropathy, cardiac failure, and pregnancy. INTERVENTIONS: After run in phase with recordings at seven weeks, three weeks, and time zero patients were allocated at random to receive moderate dietary sodium restriction for three months (n = 17) or to continue with usual diabetic diet. Subsequently nine patients in sodium restriction group continued with regimen for a further two months, during which they completed a randomised double blind crossover trial of sustained release preparation of sodium (Slow Sodium 80 mmol daily) for one month versus matching placebo for one month. END POINT: Reduction in blood pressure in type II diabetics with mild hypertension. MEASUREMENTS AND MAIN RESULTS: Supine and erect blood pressure, body weight, and 24 hour urinary sodium and potassium excretion measured monthly during parallel group and double blind crossover studies. After parallel group study sodium restriction group showed significant reduction in systolic blood pressure (supine 19.2 mm Hg, erect 21.4 mm Hg; p less than 0.001) and mean daily urinary sodium excretion (mean reduction 60 mmol/24 h). There were no appreciable changes in weight, diabetic control, or diastolic pressure. No significant changes occurred in controls. In double blind crossover study mean supine systolic blood pressure rose significantly (p less than 0.005) during sodium supplementation (to 171 mm Hg) compared with value after three months of sodium restriction alone (159.9 mm Hg) and after one month of placebo (161.8 mm Hg). CONCLUSIONS: Moderate dietary restriction of sodium has a definite hypotensive effect, which may be useful in mild hypertension of type II diabetes.

Clinical Trials as Topic↗
PubMed1986

Exploration of apical sodium transport mechanisms in an epithelial model by network thermodynamic simulation of the effect of mucosal sodium depletion: II. An apical sodium channel and amiloride blocking.

This paper is the second part of a modeling study on apical sodium transport mechanisms in tight epithelia. In the first part (this issue) we explored three expressions for the apical membrane sodium permeability (PapNa) and showed that only a PapNa which varies as a function of sodium concentration allows simulation of the well known saturation of the short-circuit current with increasing mucosal sodium concentration. However, the ad hoc expressions used have no mechanistic interpretation. We show here that if, instead of an ad hoc expression, one includes a one-site, two-barrier sodium channel in the apical membrane, the model also simulates this saturation. In addition, the equivalent apical sodium permeability computed from the simulations appears to be very similar to the phenomenological equation used by Fuchs et al. (1977) to fit the decrease of the apical sodium permeability with increasing mucosal sodium. The apical sodium channel simulated here is thus a possible mechanism for the feedback effect of the mucosal and intracellular sodium concentrations on the apical sodium permeability. This channel also allows the simulation of the competitive inhibition of the sodium current by amiloride, and the concomitant inhibition of the apical sodium permeability.

Amiloride↗
PubMed1981

Regulation of the sodium permeability of the luminal border of toad bladder by intracellular sodium and calcium: role of sodium-calcium exchange in the basolateral membrane.

Sodium movement across the luminal membrane of the toad bladder is the rate-limiting step for active transepithelial transport. Recent studies suggest that changes in intracellular sodium regulate the Na permeability of the luminal border, either directly or indirectly via increases in cell calcium induced by the high intracellular sodium. To test these proposals, we measured Na movement across the luminal membrane (th Na influx) and found that it is reduced when intracellular Na is increased by ouabain or by removal of external potassium. Removal of serosal sodium also reduced the influx, suggesting that the Na gradient across the serosal border rather than the cell Na concentration is the critical factor. Because in tissues such as muscle and nerve a steep transmembrane sodium gradient is necessary to maintain low cytosolic calcium, it is possible that a reduction in the sodium gradient in the toad bladder reduces luminal permeability by increasing the cell calcium activity. We found that the inhibition of the influx by ouabain or low serosal Na was prevented, in part, by removal of serosal calcium. To test for the existence of a sodium-calcium exchanger, we studied calcium transport in isolated basolateral membrane vesicles and found that calcium uptake was proportional to the outward directed sodium gradient. Uptake was not the result of a sodium diffusion potential. Calcium efflux from preloaded vesicles was accelerated by an inward directed sodium gradient. Preliminary kinetic analysis showed that the sodium gradient changes the Vmax but not the Km of calcium transport. These results suggest that the effect of intracellular sodium on the luminal sodium permeability is due to changes in intracellular calcium.

Animals↗
PubMed1990

Inhaled sodium metabisulphite induced bronchoconstriction: inhibition by nedocromil sodium and sodium cromoglycate.

1. The effects of nedocromil sodium and sodium cromoglycate on bronchoconstriction induced by inhaled sodium metabisulphite have been studied in eight atopic subjects, three of whom had mild asthma. 2. Nedocromil sodium (4 mg, 7.8 X 10(-6) M), sodium cromoglycate (10 mg, 24.1 X 10(-6) M) and matched placebo were administered by identical metered dose inhalers 30 min before a dose-response to sodium metabisulphite (5-100 mg ml-1) was performed. 3. Maximum fall in sGaw after placebo pre-treatment was -43.9 +/- 3.3% baseline (mean +/- s.e. mean). At the same metabisulphite concentration maximum fall in sGaw after sodium cromoglycate was -13.0 +/- 3.6% and after nedocromil sodium was +4.3 +/- 6.8%. Nedocromil sodium prevented any significant fall in sGaw even after higher concentrations of metabisulphite. 4. Both nedocromil sodium, 4 mg, and sodium cromoglycate, 10 mg, inhibited sodium metabisulphite induced bronchoconstriction but nedocromil sodium was significantly more effective. Relative in vivo potency of the two drugs is broadly in line with other in vivo and in vitro studies.

Administration, Inhalation↗
PubMed1984

The occlusion of sodium ions within the mammalian sodium-potassium pump: its role in sodium transport.

The hypothesis that the ADP-sensitive form of phosphorylated Na+, K+-ATPase contains occluded sodium ions has been tested by a procedure which involves (i) modifying the enzyme with alpha-chymotrypsin or N-ethylmaleimide (NEM) so that the ADP-sensitive form is more stable than it is in the native enzyme, (ii) phosphorylating the modified enzyme with ATP in the presence of labelled sodium ions, and (iii) forcing the phosphorylated enzyme rapidly through a cation-exchange column and measuring the labelled sodium in the effluent. The results show that ADP-sensitive phosphoenzyme prepared from alpha-chymotrypsin- or NEM-modified Na+, K+-ATPase is able to carry labelled sodium ions through a cation-exchange resin. This behaviour was not seen with native Na+, K+-ATPase or when phosphorylation was prevented by the omission of magnesium ions or by the substitution of adenylyl(beta, gamma-methylene)diphosphonate (AMP-PCP) for ATP. The occluded sodium ions were rapidly released when the phosphoenzyme was dephosphorylated by ADP. When alpha-chymotrypsin-modified enzyme was phosphorylated by ATP with 1 mM-sodium in the medium, close to three sodium ions were occluded per phospho group. The stoicheiometry at much lower sodium concentrations could not be determined satisfactorily. A consideration of the rate constants of the reactions thought to be involved in the occlusion of sodium and in the release of sodium from the occluded state shows that, so far as they are known, these constants are compatible with the hypothesis that the occluded-sodium form of the phosphoenzyme plays a central role in sodium transport through the pump.

Adenosine Diphosphate↗
PubMed1983

Sodium pump-catalyzed sodium-sodium exchange associated with ATP hydrolysis.

Inside-out red cell membrane vesicles have been used to study sodium interactions with the ATP-dependent sodium pump at sites accessible to both membrane surfaces. ATP-dependent 22Na+ influx (equivalent to efflux from cells) shows sigmoid dependence on extravesicular Na+ concentration. This is observed both in the absence of intravesicular cations and in the presence of intravesicular K or Rb ions. The kinetic behavior is similar to that observed earlier with intact cells, (Garay, R. P., and Garrahan, P. J. (1973) J. Physiol. (Lond.) 231, 297-325) and is consistent with a ratio of close to three Na ions transported per molecule of ATP hydrolyzed. With vesicles having relatively high intravesicular sodium concentration, (approximately 50 mM NaCl), the sodium pump effects an ATP-dependent sodium efflux coupled to sodium influx and to strophanthidin-sensitive ATP hydrolysis. The influx:efflux stoichiometry is approximately 1:1, and the influx:ATP hydrolysis ratio is close to 3. This ATP-dependent exchange has a higher affinity for vanadate than ATP plus ADP-dependent sodium exchange. It is concluded that this sodium-sodium exchange mode resembles sodium-potassium exchange whereby intravesicular sodium, i.e. sodium at the extracellular surface, at relatively high concentration, behaves like potassium.

Adenosine Diphosphate↗
PubMed1975

The effect of enternal sodium concentration upon sodium fluxes in Chironomus dorsalis (Meig.) and Camptochironomus tentans (Fabr.), and the effect of other ions on sodium influx in C. tentans.

In comparison with other freshwater animals, the sodium uptake mechanism in fourth instar larvae of both C. tentans and C. dorsalis has a moderate affinity for sodium. In both species half maximum influx (Km) occurs at about 0.57 mM-Na+ and is unaltered by salt depletion. Maximum influx is achieved in steady-state C. tentans at 1.9 mM-Na+, and in steady-state C. dorsalis at 3.0 mM-Na+. Both of these values increase on depletion. Efflux also appears to be saturable at higher external sodium concentrations. In C. tentans, sodium may be transported independently of chloride, although it seems likely that sodium movement is enhanced by chloride. Sulphate strongly inhibits sodium influx. Nitrate apparently inhibits sodium influx at low concentrations, but this inhibition is progressively overcome at external sodium concentrations approaching 4 mM. A number of cations interfere with sodium influx in depleted C. tentans, notably H+, Li+ and, to a lesser extent NH4+. It is suggested that these ions compete with sodium for carrier sites. Potassium is apparently transported independently of sodium.

Animals↗
PubMed2001

Final report on the safety assessment of Sodium Metaphosphate, Sodium Trimetaphosphate, and Sodium Hexametaphosphate.

These inorganic polyphosphate salts all function as chelating agents in cosmetic formulations. In addition, Sodium Metaphosphate functions as an oral care agent, Sodium Trimetaphosphate as a buffering agent, and Sodium Hexametaphosphate as a corrosion inhibitor. Only Sodium Hexametaphosphate is currently reported to be used. Although the typical concentrations historically have been less than 1%, higher concentrations have been used in products such as bath oils, which are diluted during normal use. Sodium Metaphosphate is the general term for any polyphosphate salt with four or more phosphate units. The four-phosphate unit version is cyclic, others are straight chains. The hexametaphosphate is the specific six-chain length form. The trimetaphosphate structure is cyclic. Rats fed 10% Sodium Trimetaphosphate for a month exhibited transient tubular necrosis; rats given 10% Sodium Metaphosphate had retarded growth and those fed 10% Sodium Hexametaphosphate had pale and swollen kidneys. In chronic studies using animals, growth inhibition, increased kidney weights (with calcium deposition and desquamation), bone decalcification, parathyroid hypertrophy and hyperplasia, inorganic phosphaturia, hepatic focal necrosis, and muscle fiber size alterations. Sodium Hexametaphosphate was a severe skin irritant in rabbits, whereas a 0.2% solution was only mildly irritating. A similar pattern was seen with ocular toxicity. These ingredients were not genotoxic in bacterial systems nor were they carcinogenic in rats. No reproductive or developmental toxicity was seen in studies using rats exposed to Sodium Hexametaphosphate or Sodium Trimetaphosphate. In clinical testing, irritation is seen as a function of concentration; concentrations as high as 1% produced no irritation in contact allergy patients. Because of the corrosive nature of Sodium Hexametaphosphate, it was concluded that these ingredients could be used safely if each formulation was prepared to avoid skin irritation; for example, low concentration in a leave-on product or dilution of a higher concentration as part of product usage.

Animals↗
PubMed1993

[Effect of intravenous sodium chloride load on levels of atrial natriuretic peptide (ANP) and 3'5' guanosine monophosphate (cGMP) in plasma of patients with uncomplicated sodium-sensitive arterial hypertension maintained on different dietary sodium intake].

The aim of this work was an evaluation of the effect of the acute hypervolemia induced by 90 min intravenous infusion of 1500 ml 0.9% NaCl (16.7 ml/min) on blood pressure, plasma concentration of the atrial natriuretic peptide (ANP), cyclic guanosine monophosphate (cGMP), aldosterone (ALDO), plasma renin activity (PRA) in patients with essential hypertension on the normal, low and high sodium intake. Twelve patients with noncomplicated essential sodium-sensitive arterial hypertension participated in the study. Sodium chloride infusions were performed three times: first--on the fifth day of normal daily sodium u intake (110-120 mmol/day), second--on the fifth day of low sodium intake (10-20 mmol/day), third--on the fifth day of high sodium intake (200-220 mmol/day). Acute intravenous sodium chloride load induced a significant increase of the mean arterial pressure (MBP) only when the patients were on the high sodium diet. This increase of the MBP was associated with a significantly lower increment of plasma ANP, cGMP, lower decrement of ALDO and PRA when compared to normal- or low- sodium intake. The results suggest an impairment of the adaptive homeostatic mechanisms induced by an acute intravenous sodium load in patients with noncomplicated salt-sensitive essential hypertension ingesting high-sodium diet.

Adult↗
PubMed1987

Sodium transport and the cellular sodium transport pool of colonic epithelium: effects of sodium loading, aldosterone and lithium.

The cellular sodium transport pool and sodium transepithelial fluxes were investigated in vivo in rat distal colon in relation to sodium loading by intravenous infusion (3.5 h), and to short (4 h) and prolonged (72 h) i.v. administration of aldosterone. Considerable natriuresis and increase in body sodium content were produced by the sodium load but there was no significant effect on the transcellular sodium flux (active absorption from lumen to plasma) or on the sodium transport pool. Both short and prolonged aldosteronism produced similar increases in the transport pool and in the transcellular sodium flux, but the transepithelial electrical potential difference (p.d.) was significantly greater in rats given the prolonged infusion. Addition of amiloride to the solution in the lumen of the colon almost completely abolished the p.d., the transport pool and the transcellular sodium flux of the rats receiving prolonged infusion, but had much less effect in those given the short infusion. The time-course of recovery of p.d. following prolonged aldosteronism was similar to that described for the turnover rate of rat colonic epithelial cells. Lithium within the lumen had no significant effect in untreated rats but after prolonged aldosterone infusion lithium reduced the p.d. and the transcellular sodium flux although the transport pool was not reduced. These findings are consistent with the hypothesis that aldosteronism renders the apical membranes of the epithelial cells permeable to lithium and that intracellular accumulation of lithium depresses active sodium transfer.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1996

Relative role of alkalosis and sodium ions in reversal of class I antiarrhythmic drug-induced sodium channel blockade by sodium bicarbonate.

BACKGROUND: Hypertonic sodium salts are used to treat sodium channel-blocking drug cardiotoxicity. The relative roles of alkalinization and increased sodium concentration ([Na+]o) for various drugs are incompletely known. METHODS AND RESULTS: The effects of four class I drugs on action potential characteristics of canine Purkinje fibers at equieffective concentrations (disopyramide 30 mumol/L, mexiletine 80 mumol/L, flecainide 7 mumol/L, imipramine 5 mumol/L) were studied in the presence of normal Tyrode solution and one altered solution (increased [Na+]o, increased bicarbonate concentration, or both) in each experiment. Combined increases in sodium and bicarbonate concentration significantly reduced the depressant effects of flecainide, imipramine, and mexiletine on phase 0 upstroke (Vmax) but did not alter the effects of disopyramide. The effects of sodium bicarbonate were entirely due to alkalinization in the case of imipramine, but both alkalinization and increased [Na+]o contributed to the interaction with flecainide and mexiletine. The reversal of Vmax depression by increased [Na+]o and pH was due in part to hyperpolarization. In addition, alkalosis directly reversed the hyperpolarizing shift in Vmax inactivation caused by flecainide and imipramine without altering the shift caused by disopyramide and mexiletine. CONCLUSIONS: Increases in sodium bicarbonate concentration reverse the effects of class I antiarrhythmic drugs to a varying extent, with drug-specific contributions of the sodium and bicarbonate moiety. The molecular basis for this drug specificity remains to be elucidated, but it has important potential implications for the use of hypertonic sodium salts to treat cardiotoxicity caused by sodium channel-blocking drugs.

Alkalosis↗