Sodium chloride comprises over 90% of the inorganic constituents of the blood serum. Both its ions are physiologically important. Sodium, more than any other ion, determines the osmotic pressure of interstitial fluids and the degree of hydration of tissues. When the intake of the chloride ion is less than is excreted, there is a relative increase in the blood bicarbonate level, producing the condition known as alkalosis. Other symptoms of sodium chloride deficiency are nausea, vomiting and increased irritability of muscles, evidenced by cramps and, possibly, convulsions. It is well known that excessive sweating will cause ‘‘heatcramps,’’ i.e., muscle cramps in the abdomen and extremities, which can be completely relieved only by ingestion of a weak salt solution.
Approximately 25% of the total body sodium is found in the bone. The regulation of salt and water metabolism is governed by different mechanisms; however, changes in the intake, distribution and output of salt are, in health, associated with collateral shifts of water so that electrolyte concentrations are maintained within a narrow range. In the presence of disease affecting the cardiovascular, hepatic or renal system or in certain endocrinologic disorders, changes in the rate of excretion of salt and water will disturb the homeostatic equilibrium. Frequently, abnormalities in the metabolism of water or salt may occur as a result of vomiting, diarrhea, gastrointestinal suction and fever. Excessive sweating will produce loss of water or salt, but since the electrolyte concentration is hypotonic, loss of water will predominate.
The normal salt intake ranges from 5 to 15 grams daily, most of which is excreted by the kidneys. The control of water and salt excretion in urine is very intricate, involving filtration by the glomerulus and reabsorption by the tubules of approximately 99% of the filtered load. The actual quantities excreted depends on the requirements prevailing at the moment. The finer adjustments of the tubular absorptive mechanisms are influenced by osmotic interrelationships between cell water, plasma and urine and by certain steroid hormones influencing electrolyte excretion and the posterior pituitary hormone regulating water excretion. When food intake ceases or salt is withheld, the content of sodium chloride in urine diminishes rapidly so that the body stores are retained. Similar renal retention of electrolytes occurs when salt is lost via gastrointestinal secretion through vomiting, etc. In other conditions, such as congestive heart failure, cirrhosis, nephritis or hypersecretion of the adrenal cortical hormones, the kidney fails to eliminate sufficient sodium. This results in retention of both salt and water, producing an excessive accumulation of extracellular fluid, which may be effectively combated by a sharp restriction of salt intake and use of a diuretic.
Depletion of body salt may be caused in many ways, one of which is too energetic treatment of fluid and sodium retention. Besides this, diabetic acidosis, burns, excessive sweating with free drinking of water, repeated paracentesis for removal of ascitic fluid, adrenal cortical hypofunction and certain forms of nephritis, as well as abnormal losses of gastrointestinal secretions, will cause marked salt depletion. With salt loss, there is a reduction of the osmotic pressure of the extracellular fluid; the urine volume may be retained but it is free of sodium chloride.
