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At least 19 recordsLinked to original sources
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↗
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↗
PubMed1979

Sodium-sodium exchange through the sodium pump: the roles of ATP and ADP.

1. We have developed a procedure for preparing resealed red cell ghosts that contain ADP but very little ATP. 2. The procedure involves (i) lysis of the cells in a very large volume of lysing solution, (ii) resuspension of the ghosts in a small volume, (iii) the incorporation into the ghosts, before they are resealed, of the adenylate kinase inhibitor P1,P5-di(adenosine-5'-)pentaphosphate (AP5A) and of hexokinase, and (iv) the removal of traces of ATP, formed by residual adenylate kinase activity, by the addition of glucose. 3. Measurements of sodium efflux from ghosts prepared in this way show that sodium-sodium exchange through the sodium pump does not occur in the absence of ATP even if ADP is present. 4. The beta:gamma imido analogue of ATP (AMP.PNP), which is incapable of phosphorylating sodium, potassium-ATPase, cannot replace ATP in supporting sodium-sodium exchange. 5. These findings support the hypothesis that the outward movement of sodium ions through the sodium pump is associated with the transfer of a phosphoryl group from ATP to the enzyme, and that the inward movement of sodium ions through the pump is associated with the return of a phosphoryl group from the phosphoenzyme to ADP.

Adenosine Diphosphate↗
PubMed1978

Light-scattering studies on bile acid salts I: Pattern of self-association of sodium cholate, sodium glycocholate, and sodium taurocholate in aqueous electrolyte solutions.

The pattern of association of the trihydroxy bile salts in aqueous electrolyte solutions was investigated utilizing the light-scattering technique. The turbidity of the bile salts sodium cholate, sodium taurocholate, and sodium glycocholate was determined over the concentration range of 0-25 mg/ml at 25 degrees. For sodium cholate, the concentration of the supporting electrolyte was varied from 0.15 to 0.5 M. For all bile salts in 0.15 M electrolyte, the turbidity was determined in sodium fluoride, sodium chloride, sodium bromide, and sodium iodide. Comparison of the light-scattering data with amonomer-micellar model showed that qualitative agreement was obtained; however, quantitative agreement could not be achieved. Further examination of the data showed that the light-scattering results were in good agreement with a model that includes dimers, trimers, and a higher aggregate containing approximately eight monomeric units.

Chemical Phenomena↗
PubMed1975

A comparison of natriuresis after oral and intravenous sodium loading in sodium-depleted man: evidence for a gastrointestinal or portal monitor of sodium intake.

1. Dietary sodium reduction in man is followed by rapid conservation of sodium by the kidneys. The rapidity of this response suggests that the gastrointestinal tract is involved in early recognition of changes in sodium intake or in mediation of the compensatory response. 2. In order to test the hypothesis, 100 mmol of sodium was given to normal volunteers in balance on a low-sodium diet (5 mmol/24 h): the dose was given either orally or intravenously. 3. Those who received their sodium orally excreted it more rapidly than those who received it intravenously and the difference was most marked in the first 8 h after the dose. 4. This finding is consistent with the presence of an input receptor for sodium in the gastrointestinal tract.

Administration, Oral↗
PubMedDate not supplied

[Effect of normal and high sodium diet on the sodium outflow rate through lymphocyte cell membrane and lymphocyte sodium level in patients with mild primary hypertension].

An effect of normal and high sodium diet on the rate of sodium outflow rate through lymphocyte cell membranes was evaluated in patients with mild primary hypertension with normal value of Na+ outflow rate index. It was found that high sodium value does not increase the value of this index in patients with mild primary hypertension but it does increase Na+ levels in lymphocytes. However, high sodium diet increases the value of this parameter in patients with mild primary hypertension with normal value of Na+ outflow rate through lymphocyte cell membranes and does not effect sodium level in the lymphocytes. According to the authors, high sodium diet in patients with normal renal function does not affect serum sodium levels.

Adult↗
PubMed1977

Sodium and potassium intakes and excretions of normal men consuming sodium chloride or a 1:1 mixture of sodium and potassium chlorides.

Two groups of 10 healthy young men were matched on the basis of their free-choice consumptions of regular table salt. For 28 days they were then fed carefully controlled low-sodium foods. One group was permitted free-choice seasoning of these foods with regular table salt, the other with a 1:1 mixture of sodium and potassium chlorides. Intakes and urinary and fecal excretions of sodium and potassium were determined by analysis. The results were: 1) the subjects salted their food with essentially the same amounts of regular table salt as of the 1:1 mixture; 2) the sodium intake associated with seasoning at the table was reduced with the 1:1 mixture to 44 percent of the amount consumed with regular table salt; and 3) over a 28-day period there was no tendency for subjects to increase their use of a 1:1 mixture, when used in place of regular table salt, to compensate for their reduced sodium intakes. Under the conditions of this study, the use of the 1:1 mixture as a seasoning agent for foods that contained no added salt resulted in an average total intake of sodium (food plus seasoning) which was 55 percent that of the subjects using regular table salt.

Adult↗
PubMed1976

Excretion of sodium and water by kidneys in situ and by transplanted kidneys following isotonic, hypotonic, iso-oncotic and hyperoncotic intravenous infusions in sodium-loaded and sodium-deprived dogs.

The excretion of sodium and water following isotonic, hypotonic, iso-oncotic and hyperoncotic intravenous infusions has been investigated in the kidneys in situ and in transplanted kidneys of narcotized dogs previously submitted to sodium-enriched or-deprived diets. The fractional excretion of sodium depended basically on the cumulative effect on the kidney of the changes in plasma oncotic pressure, plasma sodium concentration, and haematocrit. The differences in excretory responses of sodium-loaded or-deprived animals did not depend on differences in the distribution of infused fluids between intra- and extravascular compartments, but to the sensitivity of the kidney itself to the direct cumulative effect of these non-specific changes in blood composition.

Animals↗
PubMed1991

Sodium deficient rats are unmotivated by sodium chloride solutions mixed with the sodium channel blocker amiloride.

Rats were made sodium deficient by furosemide injection and then offered 20 min of access to 0.05 M NaCl mixed with the sodium channel blocker amiloride. Compared with a sodium deficient control group that was also offered 0.05 M NaCl, these rats drank very little. A subsequent test conducted in the same manner with 20 min of access to 0.3 M NaCl mixed with amiloride produced similar results. It is concluded that amiloride blocks the neural information required for generating the attractive taste of NaCl to the sodium deficient rat.

Amiloride↗
PubMed1978

Solubilization of napthalene by sodium cholate and pattern of self-association of sodium cholate in 0.15 M sodium chloride.

Naphthalene solubility was determined in aqueous 0.15 M NaCl containing sodium cholate in the 0-0.05 M concentration range at 25 +/- 0.1 degrees. Sodium cholate tends to self-associate in aqueous solutions. Most often, the association pattern has been described in terms of a monomer-micellar model in which it is assumed that no association occurs below the critical micelle concentration. By comparison of the experimental solubilization curve with curves calculated on the basis of the monomer-micellar model, it was shown that this model is inappropriate for the self-association pattern of sodium cholate. The solubility data were consistent with a model that assumes that sodium cholate associates to form dimers, trimers, and higher aggregates with an average aggregation number of 7.63. Model calculations suggest that naphthalene is solubilized by dimers and higher aggregates. Solubilization of naphthalene by trimers appears to be negligible.

Cholic Acids↗
PubMed1975

A comparison on natriuresis after oral and intravenous sodium loading in sodium-depleted rabbits: evidence for a gastrointestinal or portal monitor of sodium intake.

1. Rabbits in balance on a low sodium diet were given doses of sodium chloride either orally or intravenously. 2. Those receiving oral doses responded with a much greater natriuresis than those receiving intravenous ones. 3. This could be explained by the existence of a sodium input monitor somewhere in the gut or portal circulation.

Administration, Oral↗
PubMed1978

Light-scattering studies on bile acid salts II: pattern of self-association of sodium deoxycholate, sodium taurodeoxycholate, and sodium glycodeoxycholate in aqueous electrolyte solutions.

The pattern of self-association of the bile salts sodium deoxycholate, sodium glycodeoxycholate, and sodium taurodeoxycholate was investigated in aqueous electrolyte solutions by the light-scattering technique. The turbidity of the bile salt solutions was obtained over the concentration range of 0-20 mg/ml at 25 degrees. These data were analyzed according to a monomer-micellar equilibrium model and a stepwise association model. Comparison of the light-scattering data with these models suggests that the monomer-micellar model may be inappropriate. Analysis of the data according to the stepwise association model suggests that the dihydroxy bile salts associate to form dimers, trimers, and tetramers in addition to a larger aggregate which varies in size depending on the degree of conjugation of the bile salt.

Chemical Phenomena↗
PubMed1979

Sodium transport in the hen lower intestine. induction of sodium sites in the brush border by a low sodium diet.

1. The fluxes of Na were measured on isolated coprodeal mucosa at 1--220 mM-Na from hens on low (L) and high (H) Na diets with the purpose of finding the location and characteristics of Na sites activated in the cellular pathway by L. 2. The influx across the brush border, JNamc, and the transmural fluxes, JNasm and JNams, were determined. Effects on these fluxes of ouabain, 10(-3) M in the serosal solution, and amiloride, 10(-4) M in the mucosal solution, were studied for both dietary states. 3. JNamc was 5--22 (L) and 0--0.8 (H) muequiv/cm2.hr at 130 mM-Na corrected for the paracellular flux of Na. The JNamc (H) is tenfold smaller than found by Choshniak, Munck & Skadhauge (1977). This discrepancy is at present inexplicable. Amiloride completely inhibited JNamc (L). Preincubation in 0 or 130 mM-Na had no effect on JNamc. Ouabain reduced JNamc (L) by only about 37% after preincubation at 130 mM-Na. The Kt of JNamc was 5.1 (L) and 50.6 (H) mM-Na. 4. JNasm was 50 (H) and 61 (L) n-equiv/cm2.hr at 6.5 mM-Na. Ouabain increased JNasm by 360% in the low Na state. The increased JNasm was inhibited 74--100% by amiloride. This is interpreted as a ouabain induced Na-Na exchange at the basolateral Na-K-ATPase and an almost complete block of JNacm by amiloride. A similar exchange of Na at the basolateral membrane in the high-Na state was revealed by 'opening' the brush border for Na with monensin added to the mucosal solution. Amiloride in itself prevented a 50% recirculation of Na via the paracellular route and back across the cells in the low Na state. 5. JNams was 5.6 (L) muequiv/cm2.hr and 187 (L) microA/cm2 at 6.5 mM-Na. Amiloride reduced these values to 0.4 muequiv/cm2.hr and 5.8 microA/cm2. On addition of amiloride the transmural resistance in (L) coprodea at 130 mM-Na increased from 140 to 190 and it remained unchanged at 260 omega cm2 in (H) coprodea. The resistance of (L) birds, 163, was not affected by ouabain, 166 (L) omega cm2. 6. 20:1 NaCl dilution potentials at the mucosal side of 17--18 mV (L) and nearly zero (H) had half-times around 1 sec. Amiloride eliminated completely these diffusion potentials. The short half-time indicates a location in the brush border of sodium specific sites induced by the low-Na diet. This conclusion is oppsite to that described by Choshniak et al. (1977). 7. Ion selectivity, voltage--current and conductance--concentration relations in the presence of amiloride indicated a weakly cation selective and highly hydrated pathway, which was also thick and with neutral sites. This fits a paracellular route with the limiting barrier for ions at the tight junction.

Amiloride↗
PubMed1992

Effects of sodium butyrate on the expression of sodium channels by neuronal cell lines derived from the rat CNS.

We have studied the effects of sodium butyrate on cell morphology and the expression of mRNAs encoding voltage-gated sodium channels in five neuronal cell lines, B35, B50, B65, B103 and B104, all derived from the rat CNS. The cells were grown in medium supplemented with 2.5 mM sodium-n-butyrate and examined daily by phase-contrast microscopy. Sodium butyrate caused slowing of cell division and the formation of longer and more highly branched cytoplasmic processes than were present in untreated cells. Expression of sodium channel mRNA was analysed by PCR with primers that allow the transcripts encoding the different types of sodium channel to be distinguished according to the lengths of the PCR products. The identity of the PCR products was confirmed by restriction enzyme digestion. Southern blotting and hybridization with internal radiolabelled probes. Prior to sodium butyrate treatment, expression of sodium channel mRNA was largely restricted to B50 and B104 cells: B50 cells showed expression of rat brain types I and II sodium channel and B104 cells expressed rat brain type III sodium channel. After treatment for 5 days with sodium butyrate, sodium channel mRNA was detected in all five cell lines. In addition to type I and type II sodium channel, B50 cells expressed rat brain type III sodium channel. These three types of sodium channel were also expressed by B35, B65 and B103 cells. Even after butyrate treatment, B104 cells expressed only type III sodium channel. The treatment also induced expression of rat skeletal muscle SkM1 sodium channel in B35 cells but only trace amounts in the other neuronal cell lines.

Animals↗
PubMed1979

The effect of harmaline on intestinal sodium transport and on sodium-dependent D-glucose transport in brush-border membrane vesicles from rabbit jejunum.

Harmaline inhibition of sodium uptake and of sodium-dependent D-glucose transport was investigated using brush-border membrane vesicles from frozen rabbit jejunum. Under sodium-gradient conditions, "initial" D-glucose uptake (20 s) was inhibited by harmaline at concentrations above 0.5 mM, but at lower harmaline concentrations D-glucose uptake was stimulated by 10--15%. When a similar potassium gradient was used, harmaline had no effect. At concentrations up to 2 mM, harmaline did not alter the equilibrium uptake of D-glucose or D-mannitol. After pre-equilibration with sodium (25 mM), G-glucose uptake was inhibited at harmaline concentrations ranging from 0.1 to 2 mM. Sodium (10 mM) uptake was also inhibited by harmaline. Increasing the sodium concentration reduced the inhibitory effect of harmaline on tracer sodium uptake as well as on sodium-dependent D-glucose uptake. Similar to phlorizin, harmaline (1 mM) was able to prevent glucose-induced sodium influx across the brush-border membrane. Sodium uptake into brush-border membrane vesicles seems to be inhibited at lower harmaline concentrations than sodium-dependent D-glucose uptake. At high (2 mM) inhibitor concentrations, however, sodium-dependent glucose uptake is more strongly inhibited than sodium uptake. These results suggest that harmaline inhibits both sodium and sodium-dependent transport across intestinal brush-border membranes by interacting with specific sodium-binding sites.

Alkaloids↗
PubMed1977

Sodium chloride transport across the chicken coprodeum. Basic characteristics and dependence on sodium chloride intake.

1. The transport characteristics of the chicken coprodeum have been examined in vitro using the isolated mucosa. The short-circuit current (I(sc)), the transepithelial electrical potential difference (p.d.), the unidirectional transmural fluxes (J(ms), J(sm)) of sodium and chloride measured in the short-circuited state, and the unidirectional influx of sodium and chloride across the brush border membrane measured under open-circuit conditions have been studied. The effect of the sodium chloride contents of the diet on these parameters have been investigated.2. The isolated mucosa depends functionally on the presence of glucose in the incubation media. This dependence reflects the need of glucose as a fuel. There is no indication of coupling between transport of sugars and sodium across the brush border membrane. For preparations from chickens on a low sodium diet a very high and stable I(sc) can quantitatively be accounted for by the net transport of sodium. Influx of sodium across the brush border membrane is not significantly different from the net flux of sodium. By feeding the chickens a high sodium diet the I(sc) is reduced by more than 95%, the net transport of sodium is abolished, and the transepithelial electrical conductance is reduced by more than 50%.3. Both unidirectional transepithelial fluxes of chloride, and the serosa to mucosa flux of sodium appear to proceed through a paracellular shunt.4. Under the conditions of the low sodium diet the paracellular pathway appears to be anion selective. Whereas, under the conditions of the high sodium regimen the paracellular route appears to be cation selective. After adaptation to a high sodium diet the influx of sodium across the brush border membrane is only moderately reduced. Consequently the decisive event in the adaptation must be localized elsewhere.

Animals↗