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At least 127 records · Page 7Linked to original sources
PubMed1999

Assessment of sodium status in large ruminants by measuring the sodium-to-potassium ratio in muzzle secretions.

OBJECTIVE: To develop a simple diagnostic test to assess sodium status in large ruminants on the basis of the sodium-to-potassium ratio (Na:K) and to determine its relevance. ANIMALS: 7 buffalo heifers and 21 lactating, pregnant, and nonpregnant dairy cows and heifers. PROCEDURE: Buffalo heifers were subjected in 2 experiments to variable dietary sodium intake or sodium depletion and changes in sodium and potassium concentrations; Na:K was simultaneously monitored in various body fluids to study its value for indicating sodium status. Validity of the muzzle secretion test was assessed. RESULTS: Muzzle secretion and urinary Na:K and sodium concentration, but not serum electrolyte concentrations, reflected the sodium status of buffalo heifers in response to the widely variable intake of sodium (0.03 to 0.16% of dry matter [DM]). Progressive sodium depletion during an 11-day period, using saliva deprivation caused reciprocal changes in sodium and potassium concentrations in saliva and muzzle secretion, but not in urine. Decreasing urine sodium concentration was associated with decreasing urine potassium concentration. Saliva, urine, and muzzle secretion Na:K closely reflected the degree of sodium deficit. CONCLUSIONS AND CLINICAL RELEVANCE: Buffaloes or dairy cows maintained on optimal sodium intake had muzzle secretion and urine Na:K > 0.30. Muzzle secretion or urine Na:K < 0.20 or < 0.10, respectively, was indicative of sodium deficiency. Analysis of muzzle secretion Na:K, and to a large extent urine Na:K, may be used as a convenient diagnostic tool to assess sodium status in large ruminants. It has accuracy similar to that of saliva Na:K.

Animals↗
PubMed1996

Effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and metabolic parameters in elderly normotensive individuals: a randomized double-blind crossover trial.

OBJECTIVE: To examine the effect of sodium chloride- and sodium bicarbonate-rich mineral water on blood pressure and parameters of glucose and lipid metabolism in elderly normotensive individuals. METHODS: We examined 21 healthy men and women aged 60-72 years in a randomized, placebo-controlled, double-blind crossover trial. After reducing dietary salt intake to below 100 mmol/day, study participants were randomly assigned to drink 1.5 l daily of a sodium chloride-rich (sodium 84.5 mmol/l, chloride 63.7 mmol/l, bicarbonate 21.9 mmol/l), a sodium bicarbonate-rich (sodium 39.3 mmol/l, chloride 6.5 mmol/l, bicarbonate 48.8 mmol/l) and a low-sodium (placebo: sodium, chloride and bicarbonate < 0.02 mmol/l) mineral water for 4 weeks each in a three-phase crossover order. Each phase was separated by a 2-week washout period in which the study participants remained on a low-salt diet. Compliance was assessed by biweekly urinary electrolyte excretion and five study participants were excluded from analysis for failing to complete the trial or to fulfil the compliance criteria. RESULTS: Mean arterial blood pressure was significantly lower during the periods of consuming low-sodium -7.0 +/- 7.2 mmHg, P < 0.001) or sodium bicarbonate-rich (-5.7 +/- 6.4 mmHg, P < 0.05) water than at baseline. In contrast, blood pressure during the phase of drinking sodium chloride-rich water was identical to that at baseline. Ambulatory 24 h blood pressure, oral glucose tolerance and plasma lipids were not affected by the different regimens. Urinary calcium excretion was significantly reduced by drinking low-sodium or sodium bicarbonate-rich water but was unchanged under the sodium chloride-rich water. CONCLUSION: Consumption of sodium chloride-rich mineral water can abolish the blood pressure reduction induced by dietary salt restriction in elderly individuals. Sodium bicarbonate-rich mineral water in conjunction with a low-salt diet may have a beneficial effect on calcium homeostasis.

Aged↗
PubMed1985

Passive cation permeability of turtle colon: evidence for a negative interaction between intracellular sodium and apical sodium permeability.

The role of intracellular sodium in the regulation of apical sodium permeability was investigated in an electrically "tight" epithelium, the turtle colon. In the presence of low mucosal sodium (3 mM) and serosal ouabain, an inhibitor of the basolateral sodium pump, the apical membrane retained a substantial amiloride-sensitive, sodium conductance and the basolateral membrane exhibited a barium-sensitive potassium conductance in parallel with a significant sodium (and lithium) conductance. In the presence of a high mucosal sodium concentration (114 mM), however, inhibition of active sodium absorption by ouabain led to a disappearance of the amiloride-sensitive, transepithelial conductance that was due, at least in part, to a virtual abolition of the apical sodium permeability. Two lines of evidence indicate that this permeability decrease was dependent upon an increase in intracellular sodium content. First, raising the mucosal sodium concentration from 3-114 mM in the presence of ouabain reversibly inhibited the amiloride-sensitive conductance. The time course of the decline in conductance paralleled the apparent intracellular accumulation of sodium in exchange for potassium, which was monitored as a transient deflection in the amiloride-sensitive, short-circuit current. Second, the inhibitory effect of mucosal sodium-addition was markedly attenuated by serosal barium, which prevented the accumulation of sodium by blocking the electrically coupled, basolateral potassium exit. These results support the notion of a "negative feedback" effect of intracellular sodium on the apical sodium permeability.

Amiloride↗
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↗
PubMed1997

Blood volume changes during three different profiles of dialysate sodium variation with similar intradialytic sodium balances in chronic hemodialyzed patients.

The aim of this study was to evaluate the effects on blood volume (BV) preservation of three different profiles of dialysate sodium variation with similar intradialytic sodium balances. Ten uremic patients aged 50 +/- 11 years receiving regular bicarbonate hemodialysis for 49 +/- 57 months were studied. Each patient underwent three hemodialysis treatments with different modalities of dialysate sodium profiles: constant sodium hemodialysis (CHD), high-low sodium hemodialysis (H-LHD), and low-high sodium hemodialysis (L-HHD). In CHD, the dialysate sodium concentration was 141 mEq/L and did not change during treatment. In H-LHD and L-HHD, the dialysate sodium concentration at the start of dialysis was 160 mEq/L and 133 mEq/L, respectively, and remained constant for 60 minutes. At this time, a single-step break point of variation of dialysate sodium concentration occurred. The dialysate sodium concentration changed according to a model aimed to keep identical the amount of dialysate sodium exchanged in the three different dialysis procedures. The duration of hemodialysis, the blood flow rate, the dialysate flow rate, and the dialysis membrane were the same for all three different hemodialysis modalities. The ultrafiltration rate was kept constant during treatment. Total dialysate collection and intradialytic sodium balance were calculated for each hemodialysis session. Blood pressure and heart rate were monitored at 10-minute intervals; percent reductions of BV (%R-BV) were continuously monitored by an online optical reflection method (Hemoscan; Hospal-Dasco, Medolla, Italy). The results have shown a lower intradialytic %R-BV with H-LHD compared with L-HHD and CHD. No differences in total ultrafiltration rate, systolic and diastolic blood pressures, and heart rate were observed among the three different dialysis procedures. The total dialysate sodium collected and the intradialytic sodium balances were very similar among the three different dialysis procedures, confirming the accuracy of the precision of the sodium model used. The H-LHD sodium profile may be a useful tool in the prevention of excessive %R-BV and of dialysis intolerance episodes.

Adult↗
PubMed1984

Electron probe analysis of sodium and other elements in hypertrophied and sodium-loaded smooth muscle.

The composition of normal, hypertrophied, or sodium-loaded rabbit portal anterior mesenteric vein and of normal and sodium-loaded guinea pig taenia coli smooth muscle was measured in cryosections with electron probe analysis, and the effects of wash with cold sodium-free (Lithium) solutions were determined. There was no significant difference in the cytoplasmic, nuclear, or mitochondrial concentrations of any of the measured elements (sodium, potassium, chloride, magnesium, calcium, phosphorus, sulfur) between hypertrophied, sham-operated, or control veins. The cytoplasmic potassium:sodium:chloride ratio in rabbit portal anterior mesenteric vein was 1:0.26:0.46, and the average sodium concentration (198 mmol/kg dry cytoplasmic weight) was nearly twice as high as estimated from ion flux measurements. The cytoplasmic sodium concentration of normal guinea pig taenia coli was 61 mmol/kg dry weight. The existence of a rapidly exchanging, relatively low affinity, and temperature-insensitive component of cytoplasmic sodium efflux was indicated by the reduction in cytoplasmic sodium after washout in cold, sodium-free (lithium or Tris-substituted) solutions. This reduction, by 62% in normal, 71% in sodium-loaded portal anterior mesenteric vein, and 36% in sodium-loaded guinea pig taenia coli smooth muscle, suggests that the lithium wash method can underestimate cell sodium. In sodium-loaded guinea pig taenia coli and portal anterior mesenteric vein smooth muscles, the cytoplasmic sodium analyzed in individual cells showed a bimodal distribution; in cryosections, the cells having the highest sodium and lowest potassium and phosphorus content also had a more electronlucent (light cell) appearance.

Animals↗
PubMed1986

Ion transport in proximal colon of the rat. Sodium depletion stimulates neutral sodium chloride absorption.

UNLABELLED: The model of sodium and chloride transport proposed for the colon is based on studies performed in the distal segment and tacitly assumes that ion transport is similar throughout the colon. In rat distal colon, neutral sodium-chloride absorption accounts for the major fraction of overall sodium absorption and aldosterone stimulates electrogenic, amiloride-sensitive sodium absorption. Since we have demonstrated qualitative differences in potassium transport in proximal and distal segments of rat colon, unidirectional 22Na and 36Cl fluxes were performed under short-circuit conditions across isolated proximal colon of control and sodium-depleted rats with secondary hyperaldosteronism. In the control group, net sodium absorption (JNanet) (7.4 +/- 0.5 mu eq/h . cm2) was greater than Isc (1.4 +/- 0.1 mu eq/h . cm2), and JClnet was 0 in Ringer solution. Residual flux (JR) was -5.2 +/- 0.5 mu eq/h . cm2 consistent with hydrogen ion secretion suggesting that neutral sodium absorption may represent sodium-hydrogen exchange. 1 mM mucosal amiloride, which inhibits sodium-hydrogen exchange in other epithelia, produced comparable decreases in JNanet and JR (4.1 +/- 0.6 and 3.2 +/- 0.6 mu eq/h . cm2, respectively) without a parallel fall in Isc. Sodium depletion stimulated JNanet, JClnet, and Isc by 7.0 +/- 1.4, 6.3 +/- 1.9, and 0.8 +/- 0.2 mu eq/h . cm2, respectively, and 1 mM amiloride markedly inhibited JNanet and JClnet by 6.0 +/- 1.1 and 4.0 +/- 1.6 mu eq/h . cm2, respectively, with only a minimal reduction in Isc. CONCLUSIONS: the predominant neutral sodium-absorptive mechanism in proximal colon is sodium-hydrogen exchange. Sodium depletion stimulates electroneutral chloride-dependent sodium absorption (most likely as a result of increasing sodium-hydrogen and chloride-bicarbonate exchanges), not electrogenic chloride-independent sodium transport. The model of ion transport in the proximal colon is distinct from that of the distal colon.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1986

Sodium regulation of agonist binding at opioid receptors. II. Effects of sodium replacement on opioid binding in guinea pig cortical membranes.

We have examined the effects of sodium on the binding of opioid agonists to mu-, delta-, and kappa-receptors in guinea pig cortical membranes. Concentration curves for sodium indicated that maximal inhibition of mu binding by this cation was about 60% and maximal inhibition for delta binding was about 70%, whereas that for kappa binding was only about 20%. The concentration of sodium required for half-maximal inhibition of binding to all three sites was about 10-30 mM, corresponding to the intracellular sodium concentration. The nature of the sodium effect was further characterized by saturation analysis of binding to each of the three receptor types by comparing results obtained in the presence of 120 mM sodium with those obtained with equimolar replacement of sodium by another cation. Two radiolabeled agonists with different structural characteristics were tested for each binding site. In the presence of sodium, the affinity of the labeled agonists for mu sites was approximately 2-3-fold less than in its absence, but the density of binding sites was not changed. At kappa sites, sodium reduced agonist affinity slightly but, again, did not alter the number of binding sites. In contrast, sodium reduced the apparent density of delta-binding sites while leaving the agonist affinity unchanged. Competition against antagonist binding to delta sites indicated that, in the presence of sodium, a higher proportion of sites was in a lower affinity state, as reflected by the biphasic nature of the agonist displacement curve. In contrast, the effect of sodium on displacement of antagonist from mu sites was to of sodium on displacement of antagonist from mu sites was to lower the affinity of the agonist. Competition against antagonist binding to kappa sites also showed a reduction in agonist affinity by sodium, but no change in number of receptors. The results indicate that sodium may differentially regulate agonist binding to opioid receptor types and that this regulation may occur at an intracellular site. The kappa site appears to be less sensitive to sodium than the mu and delta sites.

Animals↗
PubMed1969

The influence of potassium- and sodium-free solutions on sodium efflux from squid giant axons.

The sensitivity of sodium efflux to the removal of potassium ions from the external solution and the change in sodium efflux occurring when sodium ions are also removed were observed to be related. When Tris was used to replace external sodium ions, increases in sodium efflux were always observed whether the sensitivity of sodium efflux to external potassium ions was weak or strong. Greater percentage increases in sodium efflux occurred, however, the greater the sensitivity of sodium efflux to external potassium ions. When lithium ions were used to replace external sodium ions, increases in sodium efflux occurred if the sensitivity of efflux to external potassium ions was strong whereas decreases in sodium efflux took place if the sensitivity of efflux to external potassium ions was weak. Intermediate sensitivities of efflux to external potassium resulted in no change in efflux upon substitution of lithium ions for external sodium ions. In the presence of 10(-5)M ouabain, substitution of Tris for external sodium ions always resulted in a small decrease in sodium efflux. The data can be described in terms of a model which assumes the presence of efflux stimulation sites that are about 98% selective to potassium ions and about 2% selective to sodium or lithium ions.

Animals↗
PubMed1973

Sodium uptake by frog skin and its modification by inhibitors of transepithelial sodium transport.

1. The suitability of inulin and mannitol as markers of the diffusional space that exists between the surface of frog skin and the outer barrier to sodium transport has been compared in experiments designed to measure the rapid uptake of sodium.2. Inulin and mannitol both equilibrate finally with the same space at the outer surface of the frog skin, but the rate at which this equilibration occurs is considerably faster for mannitol.3. The dependence of the rapid uptake of sodium on the concentration of sodium in the external medium, using mannitol to correct for extracellular sodium, can be described by simple saturation kinetics with an apparent K(m) for sodium entry of 24 mM and a maximal rate of uptake of 1.28 muequiv/cm(2). hr.4. The effect of amiloride is to inhibit sodium uptake, the degree of inhibition depending both on the concentration of sodium in the external medium and on the level of transepithelial transport normally maintained by the skin.5. Ouabain inhibits sodium uptake when the tissue has been pre-incubated in sodium containing medium. It has no effect on sodium uptake if the pre-incubation takes place in sodium free medium.6. A short-circuit current and potential difference can be elicited across frog skin in the presence of ouabain, by increasing the concentration of sodium bathing the outside surface. This potential and short-circuit current is abolished by the presence of amiloride.7. These results provide direct evidence that amiloride acts to stop entry of sodium into the transport compartment and suggest that the ouabain inhibition of sodium uptake is mediated primarily through an increase of epithelial sodium concentration.

Amiloride↗
PubMed1973

The effect of chronic sodium loading and sodium restriction on plasma prostaglandin A, E, and F concentrations in normal humans.

It has been suggested that prostaglandins may be involved in the control of sodium homeostasis. Prostaglandin A and prostaglandin E have been shown to increase renal blood flow and urinary sodium excretion and prostaglandin A has been shown to stimulate aldosterone release. The purpose of this study was to determine the effect of chronic sodium loading and sodium restriction on plasma prostaglandin A, E, and F concentrations. SEVEN NORMAL HUMAN VOLUNTEERS WERE PLACED ON THREE SODIUM INTAKE DIETS: (a) ad lib. sodium intake, (b) high sodium intake, and (c) low sodium intake. Plasma prostaglandin A, E, and F concentrations were measured by radioimmunoassay. Mean prostaglandin A levels on the ad lib. diet were 1.60 ng/ml. Prostaglandin A levels decreased 49% to 0.82 ng/ml on the high sodium intake and increased 34% to 2.14 ng/ml on the low sodium intake. Prostaglandin A levels increased 161% on the low sodium diet in comparison with levels on the high sodium diet. Plasma prostaglandin E and F concentrations did not change significantly during variation in sodium intake. These results show that dietary sodium content markedly effects plasma prostaglandin A levels and that prostaglandins may play a role in the physiologic mechanism of sodium homeostasis.

Adult↗
PubMed2002

Dynamics of sodium in sodium disilicate: channel relaxation and sodium diffusion.

We use molecular-dynamics computer simulations to study the dynamics of amorphous (Na2O)2(SiO2). We find that the Na ions move in channels embedded in a SiO2 matrix. The characteristic distance between these channels gives rise to a prepeak in the structure factor at q approximately equal to 0.95 A(-1). The dynamics of sodium is given by a fast process which can be seen in the incoherent scattering function and a slow process which is seen in the coherent function. The relaxation time of the latter coincides with the alpha-relaxation time of the matrix. The Kohlrausch exponent of the fast process for q>1.6 A(-1) is the same as the von Schweidler exponent for the slow one. Thus the two processes are closely related.

Journal Article↗
PubMed1981

Muzzle secretion electrolytes as a possible indicator of sodium status in buffalo (Bubalus bubalis) calves: effects of sodium depletion and aldosterone administration.

In two separate experiments, the effects of sodium depletion and aldosterone administration on sodium and potassium concentrations in muzzle secretion, saliva and urine were studied in buffalo calves. Sodium deficiency in the animals was experimentally produced by unilateral parotid saliva deprivation for 18 days. During sodium depletion, the sodium levels in saliva and muzzle secretion gradually fell while the potassium level gradually rose. The concentrations of both of these cations in urine gradually fell during the course of sodium depletion. Aldosterone administration in normal (sodium-replete) animals simulated the effects of sodium depletion as far as cationic changes in saliva were concerned. However, aldosterone did not affect sodium and potassium concentration in the urine and in muzzle secretion in a manner similar to that caused by sodium depletion. Though the hormone decreased urinary sodium without affecting urinary potassium, it did not affect the muzzle sodium or potassium. Results suggest that aldosterone affects the composition of saliva and urine in buffaloes as it does in sheep and other ruminants. Similar changes in composition of muzzle secretion and saliva during sodium depletion indicate that the concentration of sodium in muzzle secretion could possibly be used to evaluate the sodium status of animals.

Aldosterone↗