The Effects of Sodium Deprivation on the Animal Organism

Orent-Keiles, Elsa; Robinson, A.C.; McCollum, E. V.

doi:10.1152/ajplegacy.1937.119.3.651

Cited by 63 publications

(13 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…At one year of age a Swenson pull-through procedure was performed. At time of the admission, his electrolytes were as follows: sodium, 136 meq/L; potassium, 4.0 meq/L; bicarbonate, 20 meq/L; and chloride, 98 meq/L. Postoperatively, he demonstrated significant hyponatremia and hypochloremia with serum sodium concentrations as low as 120 meq/L.…”

Section: Case Reportmentioning

confidence: 99%

Diminished Linear Growth Associated with Chronic Salt Depletion

Wassner

Kulin

1990

Clin Pediatr (Phila)

View full text Add to dashboard Cite

Chronic salt depletion may be found in a variety of conditions associated with failure to thrive. Infants bom with structural renal disease may be unable to conserve sodium while those with congenital heart disease or bronchopulmonary dysplasia often require long-term treatment with potent diuretics.'-' The sodium depletion and coincident mild hyponatremia are often regarded as a secondary feature rather than as a primary contributor to the growth retardation. However, experimental evidence in both humans and animals suggests that salt depletion may in itself be responsible for decreased nitrogen balance and poor growth.4-gWe have been following a boy with long-term saltdepletion secondary to colonic resection. In this patient, sodium chloride supplementation has been associated with improved weight gain, improved height and more positive height velocity. The case is presented as an unusual cause of salt loss and as a reminder that pure salt deficiency may independently affect growth. Case ReportThe patient was referred to The Milton S. HersheyMedical Center at 48 hours of age because of intestinal obstruction. His length at birth was 53 cm (+0.9. SDSt). At laparotomy the entire large intestine was found to be aganglionic requiring colonic resection and the creation of an ileostomy. At one year of age a Swenson pull-through procedure was performed. At time of the admission, his electrolytes were as follows: sodium, 136 meq/L; potassium, 4.0 meq/L; bicarbonate, 20 meq/L; and chloride, 98 meq/L. Postoperatively, he demonstrated significant hyponatremia and hypochloremia with serum sodium concentrations as low as 120 meq/L. At discharge his serum electrolyte concentrations were: sodium 130 meq/L; potassium 5.9 meq/L; bicarbonate 20 meq/L; and chloride 91 1 meq/L. One month later, he was admitted because of postoperative ileus. At that time his electrolyte values were: sodium 119 meq/L, potassium 5.5 meq/L, Co2 21 1 meq/L, and chloride 83 meq/L. The patient was lost to follow-up but returned at age seven years, when he was again referred because of poor growth. Despite height and weight measurements being below the 5th percentile (see table), an evaluation was not performed. He was again seen at age nine years for the same complaint. History revealed two to three semi-liquid stools/day and the lack of permanent dentition. The parents reported that he salted his food liberally but could not quantitate this craving more objectively. His length at 11 months of age was 72.5 cm (-0.9 SDS) and by 18 months of age he grew to only 77 cm (-2.0 SDS). Family history included father's and mother's heights of 165.1 I and 160 cm respectively and four siblings whose growth was normal for age. There was a paternal grandfather who became deaf in mid-life and the patient's father was hypothyroid and receiving replacement medication. t SDS, in this case the standard deviation score for height, is calculated as the mean height (X) at that age minus the patient's height (xp) divided by the standard deviation of the mean height (SDd-SDS=(...

show abstract

Section: Case Reportmentioning

confidence: 99%

Diminished Linear Growth Associated with Chronic Salt Depletion

Wassner

Kulin

1990

Clin Pediatr (Phila)

View full text Add to dashboard Cite

show abstract

“…When body fluids are lost, blood volume cannot be restored by drinking water alone; sodium must be ingested as well (McCance, 1936;Nose et al, 1988). Sodium deficiency causes severe deficits in growth and reproduction (Fine et al, 1987), and, ultimately, a salt-free diet is lethal (Orent-Keiles et al, 1937).…”

Section: Introductionmentioning

confidence: 99%

Aldosterone Target Neurons in the Nucleus Tractus Solitarius Drive Sodium Appetite

Geerling¹,

Engeland²,

Kawata³

et al. 2006

J. Neurosci.

135

187

View full text Add to dashboard Cite

Sodium appetite can be enhanced by the adrenal steroid aldosterone via an unknown brain mechanism. A novel group of neurons in the nucleus tractus solitarius expresses the enzyme 11-␤-hydroxysteroid dehydrogenase type 2, which makes them selectively responsive to aldosterone. Their activation parallels sodium appetite in different paradigms of salt loss even in the absence of aldosterone. These unique aldosterone target neurons may represent a previously unrecognized central convergence point at which hormonal and neural signals can be integrated to drive sodium appetite.

show abstract

“…While physicians often ascribe the growth failure to the underlying disease, evidence exists to implicate the salt depletion per se as an etiology of growth failure. Studies in both experimental animals and humans have documented that, in spite of normal caloric intake, salt deficiency is associated with decreased weight and length gain [5] and diminished nitrogen balance [5,6]. A recent report from this laboratory has demonstrated, that in addition to its role in the maintenance of extracellular space, young rats made sodium deficient demonstrate diminished rates of muscle protein synthesis, decreased nitrogen balances and decreased muscle RNA concentrations [7].…”

Section: Introductionmentioning

confidence: 99%

The effect of sodium repletion on growth and protein turnover in sodium-depleted rats

Wassner

1991

Pediatr Nephrol

View full text Add to dashboard Cite

This study examines the consequences of sodium chloride supplementation to young rats previously made salt deficient by feeding them a sodium-deficient, chloride-replete diet. Salt-deficient rats received the test diet and distilled water for 10 days. As in our previous studies, rats cared for in this manner grew more slowly than rats fed the identical diet but allowed to drink 37 mM sodium chloride. On day 11, half of the salt-depleted animals received 37 mM sodium chloride in their drinking water. Sodium-deficient and supplemented rats were studied 1,2,5-6 and 11-12 days later. Urinary sodium rapidly rose from undetectable of 46 mEq/l urine within 1 day of supplementation and there was no further increase the next day, suggesting that extracellular fluid volumes were rapidly repleted. Food intake increased in the supplemented rats compared with the deficient animals but the difference in food intake equalled only 2.25 g/day for the first 2 days of supplementation. Over the last 12 days of the study, the slopes of both weight and length gains were equal in both the supplemented and the control group and significantly higher than those in the deficient rats. Over the course of the study, full catchup was not obtained in either length or weight. In addition to total weight and length gains, liver and kidney weights increased proportionately and by 5-6 days of supplementation were equivalent to the weights seen in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

The Effects of Sodium Deprivation on the Animal Organism

Cited by 63 publications

References 0 publications

Diminished Linear Growth Associated with Chronic Salt Depletion

Diminished Linear Growth Associated with Chronic Salt Depletion

Aldosterone Target Neurons in the Nucleus Tractus Solitarius Drive Sodium Appetite

The effect of sodium repletion on growth and protein turnover in sodium-depleted rats

Contact Info

Product

Resources

About