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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To further delineate the effects of fasting and sodium deprivation on the handling of sodium when sodium intake is resumed, balance studies were performed on seven obese female subjects. All subjects underwent a period of total fasting, which continued for 27 to 29 days prior to resumption of sodium intake. Natriuresis in the first week of fasting and continued sodium chloride deprivation resulted in cumulative deficits of 383 +/- 47 mEq (SEM) and 371 +/- 41 mEq of sodium and chloride, respectively. Chloride space decreased from 21.2 +/- 2.7 L to 18.7 +/- 2.5 L, and aldosterone secretory rates (ASR) increased from 43 +/- 13 micrograms/24 h to 597 +/- 138 micrograms/24 h. Following resumption of sodium intake and simultaneous refeeding on low calorie diets in studies on four subjects (group I), cumulative sodium balances during the first seven days ranged from +586 mEq to +1,109 mEq; sodium retained/previously existing sodium deficit = 2.4, 3.2, 2.0, and 1.6 in the four subjects, respectively. Continued sodium retention resulted in cumulative sodium balances ranging from +670 mEq to +1,249 mEq at the end of 19 to 22 days in studies on three subjects whose cumulative sodium balance was +1,249 mEq, sodium retained/sodium deficit = 3.6. During the first five days of sodium intake and refeeding ASR decreased to 74 +/- 26 micrograms/24 h. Sodium chloride administration without refeeding in studies on three subjects (group II) also resulted in retention of more than enough sodium to replenish previously existing sodium deficits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies of marked and persistent sodium retention in previously fasted and sodium-deprived obese subjects. 360 Feb 74

An epidemiological study was conducted in the market town of March, Cambridgeshire, to assess the quantitative importance of cooking and table salt to total dietary salt intake by the use of a fused mixture of lithium carbonate and sodium chloride. Men and women aged 20-60 participated in a 12 day study with sequential 24 h urine collections to assess salt sources over a 7 day period. Total salt consumption estimated from urinary chloride excretion amounted to 10.6 +/- 0.55 (SEM) g in 33 men and 7.4 +/- 0.29 (SEM) g in 50 women. The cooking salt eaten was only 0.45 +/- 0.09 (SEM) g in men and women, with men eating more table salt (0.77 g/day) than women (0.46 g/day). Discretionary sources, i.e. cooking and table salt use, contributed only 15% to the total intake. Salt from manufacturing foods and catering in purchased food therefore provided on average 85% of total salt intake. These results are consistent even when an allowance is made for the slightly poorer pouring quality of the lithium-tagged salt. The importance of food as a source of salt was reflected in the significant relationship between the weight of the individual and the amount of salt eaten (for males P less than 0.05 and for females P less than 0.001). Cooking salt consumption did not relate to the amount of salt derived from purchased food nor did table salt use relate to the amount of salt in cooked foods.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:An assessment of the sources of dietary salt in a British population. 380 26

Eighteen moderately obese middle-aged men with untreated mild hypertension were randomized to two groups and placed on a low energy diet regimen for 9 to 11 weeks. In Group I (n = 10) the amount of sodium chloride in the diet maintained the urinary sodium excretion at the predieting level. Mean body mass was reduced by 9.1 +/- 0.7 (SEM) kg. Mean intra-arterial pressure showed no significant change. There were significant decreases in heart rate (p less than 0.05) and urinary norepinephrine excretion (p less than 0.05) but not in plasma concentration of norepinephrine. In Group II (n = 8) energy as well as sodium intake was restricted, with a 95 +/- 22 mmol/24 hour reduction of urinary sodium excretion. Body mass decreased by 9.3 +/- 1.1 kg, and mean arterial pressure decreased by -18.9 to -4.3 mm Hg (95% confidence interval). There were also significant reductions in heart rate (p less than 0.001) and plasma norepinephrine concentrations (p less than 0.01) but not in urinary norepinephrine excretion. The pressor response (mean arterial pressure) to norepinephrine infusion at different dose rates was significantly elevated (p less than 0.05) in Group I during dieting in comparison with baseline. The blood pressure response to norepinephrine during dieting in patients in Group II was not changed from baseline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reactivity to norepinephrine and effect of sodium on blood pressure during weight loss. 389 15

We compared the ionic activity of sodium, as measured with glass electrodes, with sodium concentration in 23 healthy persons, 15 persons with acute renal failure, and before and after dialysis in 46 patients with chronic renal failure. In healthy persons the mean (+/- SEM) sodium concentration was 139.1 +/- 0.6 mmol/L, whereas the ionic activity was equal to that of a 145.2 +/- 0.5 mmol/L solution of sodium chloride. Variation in the concentration of plasma protein was the most important factor influencing the sodium activity coefficient (the ratio between activity and concentration). The sodium activity coefficient in plasma water (corrected for the non-aqueous phase of the plasma) was fairly constant, being 96% of that in a 140 mmol/L solution of sodium chloride. Thus sodium binds to non-protein molecules and sodium ions interact with other substances in uremic plasma only to a very limited extent. The sum of the molar activities of sodium, potassium, urea, and creatinine was closely and linearly correlated with plasma osmolality, both before and after dialysis.
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PMID:Sodium activity, sodium concentration, and osmolality in plasma in acute and chronic renal failure. 405 50

It has been suggested that glucagon-like immunoreactivity (GLI) of gastrointestinal tissues might, like pancreatic glucagon, have calcium-lowering activity. Studies were designed, therefore, to determine if calcium absorption was associated with GLI release from the gut. The intraduodenal administration of 4.5 mmoles of calcium chloride per kg of body weight to conscious dogs was associated with a prompt rise in plasma GLI from a base line of 2.2 ng/ml (SEM +/-0.2) to a peak of 4.3 ng/ml (SEM +/-0.3) at 45 and 60 min, in association with a rise of plasma calcium from 8.6 to 10.4 mg/100 ml. Neither pancreatic glucagon, insulin, nor glucose changed. Smaller calcium loads had progressively diminishing effects on GLI release. Calcium lactate also appeared to stimulate effectively GLI release. Both magnesium chloride and sodium chloride given intraduodenally were associated with a significant though modest increase in GLI. To determine if stimulation of GLI release by substances other than calcium would lower serum calcium, glucose was administered intraduodenally. Despite a marked increase in GLI, plasma calcium fell only 9%, a decline which could be entirely accounted for by hemodilution. Although the physiologic significance of this demonstration that the absorption of calcium salts is associated with GLI release is open to serious question, the findings are not incompatible with the concept that glucagon-like polypeptides are released from the gut during the absorption of certain salts, possibly to alert appropriate homeostatic regulators so as to avoid major changes in electrolyte concentration after the ingestion of large salt loads.
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PMID:The effect of calcium and other salts upon the release of glucagon-like immunoreactivity from the gut. 501 13

An organ culture system of a male guinea pig hypothalamo-neurohypophyseal complex (HNC) was established. On day 5 in culture, (Na+ -K+) ATPase activity was 0.83 +/- 0.11 mM Pi/mg prot/hr (mean +/- SEM): that is 67% of that on day 1 in culture. 3H-thymidine incorporated into DNA in the explants of HNC was 1,205 +/- 185 cpm/microgram DNA. The explants responded to the elevated KCl medium and the hypertonic solution of sodium chloride with a 470 +/- 38% and 298 +/- 31% increase in arginine vasopression (AVP) release, respectively. This response was inhibited by the addition of tetrodotoxin to the culture medium. AVP release from the explants in res-onse to angiotensin II increased significantly in a dose dependent manner. [Sar1, Ile8] angiotensin II, however, attenuated the response of the explants to angiotensin II when administered simultaneously with angiotensin II. These results suggest that angiotensin II and its analogue cause the AVP release from the explants in a competitive manner. The concentrations of AVP in the culture media made hypertonic with sodium chloride, sucrose and mannitol were 298 +/- 31% (p less than 0.01), 251 +/- 36% (p less than 0.01) and 255 +/- 59% (p less than 0.05) of their control values, respectively. The hypertonic solutions of sodium chloride, sucrose and mannitol caused AVP release from the explants in vitro, while the hypertonic solutions of glucose and urea were revealed to be poor osmotic stimuli on AVP release. These results support the concept of osmoreceptors to release AVP from the hypothalamo-neurohypophyseal axis.
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PMID:[Osmotic pressure and angiotensin II stimulation of arginine vasopressin release from a guinea pig hypothalamo-neurohypophyseal complex in organ culture (author's transl)]. 644 94

The element concentrations in various intra- and extracellular compartments of the tip of the rat renal papilla were determined during antidiuresis using electron microprobe analysis. Urinary concentrations (means +/- SEM) were: urea, 1509 +/- 116; potassium, 268 +/- 32; sodium, 62 +/- 19 mmoles X 1(-1); and osmolality, 2548 +/- 141 mOsm X kg-1. Electrolyte concentrations in the interstitial space were: sodium, 437 +/- 19; chloride, 438 +/- 20; and potassium, 35 +/- 2 mmoles X kg-1 wet wt. The vasa recta plasma exhibited almost identical element concentrations. The values in the papillary collecting duct cells were: sodium, 28 +/- 1; chloride, 76 +/- 3; potassium, 135 +/- 3; and phosphorus, 316 +/- 7 mmoles X kg-1 wet wt. Similar concentrations were observed in the papillary epithelial cells. In interstitial cells potassium and phosphorus concentrations were virtually identical to those of the collecting duct cells, whereas sodium and chloride concentrations were higher by about 30 mmoles X kg-1 wet wt. The element composition of the various papillary cells is, thus, not substantially different from that of proximal tubular cells. This finding demonstrates that cellular accumulation of electrolytes is not the regulatory mechanism by which papillary cells adapt osmotically to their high environmental osmolality and sodium chloride concentration.
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PMID:Intra- and extracellular element concentrations of rat renal papilla in antidiuresis. 672 35

We have previously reported that hyperosmotic solutions of sodium chloride or of xylitol possess potent anti-ulcer activity and reduce gastric acidity in the rat. They also stimulate gastric prostaglandin (PG) biosynthesis, which may bear a causal relationship to the above effects. In the present investigation we studied the effect of intragastric hyperosmolarity on the transmucosal potential difference (PD) and on the permeability to H+ ions in the rat stomach. We also studied the effect of the prostaglandin synthetase inhibitors, indomethacin and flufenamic acid, on these parameters. Rat stomach was perfused in vivo, under urethane anesthesia, by xylitol solutions made up in 0.01 N HCl. While moderately hyperosmotic (13%) xylitol was without effect, the perfusion of intensely hyperosmotic xylitol (34.5%) resulted in a long lasting reduction of the transmucosal PD from a mean (+/- SEM) of -63 +/- 4 mV to a trough value of -40 +/- 3 mV. This depression of transmucosal PD was inhibited in a dose-related fashion by prior treatment with the PG-synthetase inhibitors. Acid recovery in the effluent was significantly reduced by the 34.5% xylitol solution and indomethacin pretreatment did not modify the effect of hyperosmotic xylitol. It is concluded that, although intensely hyperosmotic xylitol produces some of the characteristic effects of a barrier breaker, i.e. depression of transmucosal PD and acid back diffusion, these two phenomena probably involve different mechanisms, as indicated by their differential response to indomethacin.
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PMID:Hyperosmotic xylitol, prostaglandins and gastric mucosal barrier. 679 43

1. The effects of changes in sodium balance on renal prostaglandins have been hitherto studied mainly in experimental animals and the results have been controversial. In this study the 24 h urinary excretion of prostaglandins E2 and F2 alpha was measured by radioimmunoassay in seven normal subjects under basal conditions and after 5 days of a diet containing less than 20 mmol of sodium/day. Subsequently a sodium chloride (150 mmol/l: saline) load (300 mmol of sodium over 4 h) was infused and prostaglandins were again measured in hourly urine collections. Plasma renin activity and aldosterone were also measured under basal conditions, after the low sodium diet and at 2 and 4 h of the saline infusion. 2. Dietary sodium restriction was associated with a marked increase in prostaglandin E2 excretion (from 769.7 +/- 201.6 SEM to 1761.3 +/- 304.9 ng/24 h, P less than 0.0005). Prostaglandin F2 alpha also increased from 1187.0 +/- 390.1 to 1435.6 +/- 344.6 ng/24 h, but this was not statistically significant. The prostaglandin E2/prostaglandin F2 alpha ratio increased from 0.83 +/- 0.2 to 1.52 +/- 0.34 (P less than 0.01). Plasma renin activity and aldosterone rose significantly (P less than 0.05 and less than 0.0025 respectively). 3. During the saline load prostaglandin E2 decreased after 2 h from 142.4 +/- 29.9 to 86.7 +/- 22.9 ng/h (P less than 0.05) and to 36.9 +/- 5.96 ng/h after 4 h. Prostaglandin F2 alpha decreased at a slower rate, from 98.4 +/- 18.7 to 37.5 +/- 8.8 ng/h at 4 h (P less than 0.02). At 4 h the prostaglandin E2/prostaglandin F2 alpha ratio returned to control values (0.90 +/- 0.17). Plasma renin activity and aldosterone decreased significantly after 2 h (P less than 0.02 and less than 0.0025 respectively) and reached control values after 4 h. 4. The present study demonstrates that chronic and acute changes in sodium balance induce changes in the excretion of prostaglandin E2 parallel to changes in plasma renin activity and aldosterone. The similar but quantitatively smaller changes in prostaglandin F2 alpha and the inversion of the ratio between the two prostaglandins during sodium deprivation suggest that at least two factors are involved: increased delivery of substrate for prostaglandin synthase and decreased activity of the prostaglandin E1 9-keto-reductase. Prostaglandins probably play an important role in the adaptation of the kidney to changes in sodium balance.
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PMID:Effect of chronic and acute changes in sodium balance on the urinary excretion of prostaglandins E2 and F2 alpha in normal man. 701 97

Severe hyponatremia with hypoosmolality carries a high morbidity and mortality and constitutes a life-threatening emergency. We report seen cases of severe hyponatremia (serum sodium concentration 99.7 +/- 3.0 meg/liter) (mean +/- SEM) with hypoosmolality (212 +/- i mOsm/kg water) that presented with severe neurologic complications. Serum sodium concentration was corrected in 13.3 +/- 2.2 hours to mildly hyponatremic levels (serum sodium concentration 128.3 +/- 1.6 meq/liter). The rate of correction of serum sodium concentration was 2.4 +/- 0.5 meq!liter/hr. This was achieved by the intravenous administration of 3 percent hypertonic saline solution (687 +/- 43 meq sodium chloride) and furosemide or by hemodialysis where indicated. No complications occurred from treatment and all of our patients recovered without neurologic sequelae. Early diagnosis and rapid correction of serum sodium concentration appear to reduce the significant morbidity and mortality of severe hyponatremia.
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PMID:Rapid correction of severe hyponatremia with intravenous hypertonic saline solution. 705 21


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