Effect Of Sodium Deficiency Research Articles

Effect of sodium deficiency on the critical behavior near the paramagnetic to ferromagnetic phase transition temperature in La0.8Na0.2−x□xMnO3 oxides

The critical behavior associated with the magnetic phase transition has been investigated by in La0.8Na0.2−x□xMnO3 (0.00≤x≤0.15) (□ is the sodium deficiency). The critical exponents are estimated by various techniques such as the modified Arrott plot, Kouvel–Fisher plot and critical isotherm technique. Compared to standard models, the critical exponent values determined in our work are close to those expected by the tricritical model (β=0.25, γ=1, and δ=5) for x=0.00 and 0.05 samples and by mean field theory (β=0.5, γ=1, and δ=3) for x=0.10 and 0.15 samples. We conclude that the Na deficiency rate affect the critical exponents.

Sodium deficiency effect on the transport properties of La0.8Na0.2−x□xMnO3 manganites

Effect of sodium deficiency on the transport properties of La0.8Na0.2−x□xMnO3 manganites is investigated using impedance spectroscopy technique. In the whole explored temperature range (77–700K), conductivity measurements show the appearance of a metal–semiconductor transition for all investigated samples. Also, a saturation region is observed in σ (T) curves. It is found that conduction mechanism is governed by hopping process. The conductivity of the material decreases with increasing sodium deficiency. The transition temperature and the activation energy values inferred from grain boundary resistance and conductivity analysis are closed to each other. Such result confirms the contribution of grain boundary on the electrical conductivity. The variation of the Average Normalized Change (ANC) and its derivative with temperature gives important information about the available density of trapped charge states. The obtained results explain the observed saturation region in conductivity at high temperature region.

The biopsychology of salt hunger and sodium deficiency.

Sodium is a necessary dietary macromineral that tended to be sparsely distributed in mankind's environment in the past. Evolutionary selection pressure shaped physiological mechanisms including hormonal systems and neural circuits that serve to promote sodium ingestion. Sodium deficiency triggers the activation of these hormonal systems and neural circuits to engage motivational processes that elicit a craving for salty substances and a state of reward when salty foods are consumed. Sodium deficiency also appears to be associated with aversive psychological states including anhedonia, impaired cognition, and fatigue. Under certain circumstances the psychological processes that promote salt intake can become powerful enough to cause "salt gluttony," or salt intake far in excess of physiological need. The present review discusses three aspects of the biopsychology of salt hunger and sodium deficiency: (1) the psychological processes that promote salt intake during sodium deficiency, (2) the effects of sodium deficiency on mood and cognition, and (3) the sensitization of sodium appetite as a possible cause of salt gluttony.

Effect of sodium deficiency on growth of surgical infants: a retrospective observational study.

Background/aimSodium is thought to be critical to growth. Infants who have an ileostomy may suffer from growth faltering, as sodium losses from stomas may be excessive. Urinary sodium measurements may indicate which patients could benefit from sodium supplementation; however, there is no consensus on what level of urinary sodium should be the cutoff for intervention. Our aim was to determine whether there is a relationship between urinary sodium and growth in infants undergoing ileostomy, colostomy and cystostomy.MethodsFollowing audit approval, a retrospective observational study of patient notes and chemical pathology data was carried out. All infants <1 year of age that had an ileostomy, colostomy, or cystostomy procedure between February 1997 and January 2014 were included. Patients’ weights, urinary and serum sodium and potassium levels and clinical variables were recorded until discharge. Weights were converted to Z-scores for analysis.ResultsForty patients were identified whose notes were available for review and who had at least three urinary sodium measurements. During their hospital stay, 11 (28 %) maintained weight within normal limits (Z-scores −2 to +2, 15 (38 %) were moderately malnourished (−3 to −2) and 14 (35 %) severely malnourished (<−3). Thirty patients had at least one urinary sodium <10 mmol/litre, six patients had their lowest recorded urinary sodium between 10 and 30 mmol/litre and only four patients had all their urinary sodium measurements >30 mmol litre. Electrolyte data were not normally distributed so that correlations between electrolytes and growth were tested using the non-parametric Spearman rank correlation coefficient. Urinary sodium levels positively correlated with growth (r = 0.3071, p < 0.0001), as did serum sodium levels (r = 0.2620, p = 0.0059) whereas there was no relationship between urine or serum potassium and growth.ConclusionsPoor growth is frequent in this group of patients and appears to be linked with sodium levels. Further work is necessary to draw up guidelines for appropriate sodium supplementation.

Effets de la carence en sodium sur la cytologie de la cyanobactérie Anabaena cylindrica Lemm

The effects of sodium deficiency on the distribution and the ultrastructural aspect of the various cell types in the filaments were studied during growth of Anabaena cylindrica (strain 1403/2A) in presence of different amounts of nitrate (0, 1 or 10 mequiv./L). Visible symptoms such as chlorosis and reduced growth were clearly apparent several days after inoculation only when nitrate was present in the medium. The filaments broke up and contained exclusively vegetative cells rich in polyglucan granules and showing ultrastructural analogies with akinetes. In absence of sodium increasing nitrate uptake and nitrite efflux were observed in nitrate-enriched cultures (10 mequiv./L). The amount of excreted nitrite was too low to explain the described disturbances. The needs for sodium were lower for cultures without added nitrate. However, whatever the medium, the sodium deficiency brought about a delay in heterocyst differentiation without detrimental effect to the further development of cultures.Key words: cyanobacterium, Anabaena cylindrica, sodium deficiency, heterocyst differentiation, akinete differentiation, ultrastructural changes, nitrate uptake, nitrite efflux.

A Role for β-Melanotropin in the Regulation of Aldosterone Secretion during Sodium Deficiency in the Rat

1. The effect of sodium deficiency on adrenal sensitivity to β-melanotropin (β-melanocyte stimulating hormone; β-MSH) and the effect of β-MSH on a late step of aldosterone biosynthesis were studied using collagenase-dispersed rat adrenal cells. 2. Sodium depletion enhanced the sensitivity of the adrenal glomerulosa cells to β-MSH, resulting in a shift of the dose-response curve to the left, so that doses of β-MSH within the physiological range caused significant stimulation of aldosterone production. 3. The aldosterone level obtained by maximum doses of β-MSH was similar to that obtained after angiotensin (‘angiotensin II’; ANGII) during sodium depletion. 4. Sodium depletion did not change the corticosterone response to β-MSH by decapsular cells. 5. Similarly to ANGII, β-MSH significantly stimulated the conversion of exogenous corticosterone into aldosterone in the presence of an inhibitor of 3β-hydroxysteroid dehydrogenase, WIN 19,578. 6. These data suggest that β-MSH or peptides containing β-MSH may play a role in the regulation of aldosterone secretion during sodium depletion in the rat and that β-MSH increases aldosterone production partly by stimulating the late step in aldosterone biosynthesis, the conversion of corticosterone into aldosterone.

Effects of sodium deficiency on sodium saccharin drinking

This experiment attempts to test Warren & Warren’s (1966) hypothesis that the persistence of intake of nonnutritive sodium saccharin is due in part to the sodium content of the solution. The intakes of sodium saccharin, sodium chloride, and deionized water by sodium-sufficient and by sodium-deficient rats were compared, using a single-stimulus technique. The results contradict Warren and Warren’s findings, leading to the conclusion that sodium does not play an important role in saccharin preference.

Effects of sodium deficiency, potassium deficiency and uremia upon the steroidogenic response of rat adrenal tissue to serotonin, potassium ions and adrenocorticotropin.

Quartered adrenal glands of rats kept on a sodium-deficient diet or uremic after bilateral nephrectomy were found to produce more aldosterone and less deoxycorticosterone in vitro than adrenal tissue of normal rats. On the other hand, dietary potassium deficiency led to a decreased aldosterone production and an increased deoxycorticosterone production. These differences in corticosteroid production became especially marked when the adrenals were stimulated in vitro by serotonin, adrenocorticotropin (ACTH) or a high potassium concentration in the incubation medium. In adrenals of sodium-deficient or uremic rats aldosterone production was stimulated to the same extent by the addition of progesterone, deoxycorticosterone or corticosterone, whereas in normal adrenal tissue aldosterone production was highest when corticosterone was added to the incubation medium. Only added corticosterone significantly stimulated aldosterone production in adrenals of potassium-deficient rats. These results indicate that the st...

Sensitivity to angiotensin and adrenocorticotrophic hormone in the sodium deficient rat.

The effect of sodium deficiency, produced by 1 week of dietary salt restriction, on the adrenal response to angiotensin and adrenocorticotrophin (ACTH), singly and together, has been studied in acutely hypophysectomized-nephrectomized rats. Adrenal response was determined by the rate of secretion of aldosterone and corticosterone into adrenal vein blood as measured by the double isotope method. In sodium replete animals angiotensin did not significantly influence the secretion rate of either hormone. In sodium deficient animals it produced a significant increase in the secretion rate of aldosterone but not corticosterone. ACTH produced a significant increase in the secretion rates of both hormones. The response was similar in sodium replete and sodium deficient animals. When infused together in sodium replete animals the effect was no greater than with ACTH alone. However, when both hormones were infused together into sodium deficient animals the response in aldosterone secretion was even greater than the sum of the responses produced separately. Corticosterone secretion was no greater than it was with ACTH alone, regardless of previous diet. It is concluded that sodium deficiency in the rat sensitizes the aldosterone secreting mechanism to angiotensin but does not increase its sensitivity to ACTH. The synergistic effect on aldosterone secretion observed in the sodium deficient animals may be explained as a potentiation of the angiotensin effect by the increased availability of precursors when ACTH is infused at the same time. The present studies indicate that after 1 week of dietary salt restriction the adrenal cortex is sufficiently sensitive to angiotensin to allow for the demonstration of a significant effect on the secretion rate of aldosterone by the infusion of modest amounts of the hormone. The results support the view that angiotensin is involved in the adrenal response to sodium deficiency in the rat. (Endocrinology83: 1108, 1968)

Effect of sodium deficiency on cochlear potentials.

The scala tympani in guinea pigs was prefused with mammalian Ringer-Locke's solution, in which NaCl was replaced with either choline chloride or sucrose. Cochlear potentials were recorded from the basal turn before, during, and subsequent to the perfusion. Complete replacement of the perilymph with Na+-free solution did not alter the endocochlear potential and the cochlear microphonic immediately, although the action potential was abolished rapidly. In most cases, the depression of the action potential was reversible. The mechanism underlying the generation of the receptor potential is discussed, and it is concluded that production of cochlear microphonic is not dependent on the concentration of Na+ in the perilymph but on the presence of high K+ concentration in the endolymph.

The Effect of Sodium Deficiency on Cochlear Potentials

The scala vestibuli and/or scala tympani in guinea pigs were perfused with Na+ free Locke's solution, in which NaCl was replaced with either choline chloride or sucrose. Cochlear microphonics (CM), summating potential (SP), action potential (AP), and endocochlear potential (EP) were recorded from the basal turn before, during, and subsequent to, the perfusion. Complete replacement of the perilymph with Na+-free solution did not alter EP and CM immediately, although AP was abolished rapidly. Lack of Na in the perilymph of scala tympani depressed AP more markedly than did a comparable deficiency in scala vestibuli. In most cases, the depression of AP was reversible and EP and CM showed a gradual decline after the perfusion. These data were further confirmed by the fact that tetrodotoxin at a concentration of 50λ/l did not modify EP and CM, although AP was abolished promptly. The mechanism underlying the generation of the receptor potential is discussed. [Work supported by National Institutes of Health, Public Health Service, U. S. Department of Health, Education and Welfare.]

Effect of sodium-deficiency on the membrane activity of the frog's heart.

AbstractIt was shown in these experiments that the minimum sodium concentration for electrical activity of the frog heart is below 10% if at the same time potassium, calcium and chloride concentrations are reduced. Action potentials with nearly normal amplitude and duration were obtained in an isotonic sucrose solution containing only 4.8 mM. sodium (4.2% of the normal).The presence of potassium, calcium or chloride decreases the action potential and finally makes the tissus inexcitable. An increase in amplitude of the action potential was observed in the presence of 10−6 adrenaline. To explain this action stimulation of the cation transport mechanism is proposed.

Stress and cardiac infarcts. Effect of sodium deficiency upon necrotizing cardiopathies produced by various agents.

Stress and cardiac infarcts. Effect of sodium deficiency upon necrotizing cardiopathies produced by various agents.