Introduction

Salt (sodium chloride) is essential for life. The tight regulation of the body's sodium and chloride concentrations is so important that multiple mechanisms work in concert to control them. Although scientists agree that a minimal amount of salt is required for survival, the health implications of excess salt intake represent an area of considerable controversy among scientists, clinicians, and public health experts.

Sodium (Na+) and chloride (Cl-) are the principal ions in the fluid outside of cells (extracellular fluid), which includes blood plasma. As such, they play critical roles in a number of life-sustaining processes.

Food Sources

Most of the sodium and chloride in the diet comes from salt. The lowest salt intakes are associated with diets that emphasize unprocessed foods, especially fruits, vegetables, and legumes.

Minerals from plant sources may vary from place to place because soil mineral content varies geographically.

Some important food sources of Sodium

Salami	Ham	Ketchup	Bread	Corn flakes
Pretzels	Potato chips	Soup	Bacon	Hot dog

Recommended Dietary Allowance (RDA)

The European Union and the US have not set a RDA for the general population.

Functions in the Body

Maintenance of membrane potential

Sodium and chloride are electrolytes that contribute to the maintenance of concentration and charge differences across cell membranes. Potassium is the principal positively charged ion (cation) inside of cells, while sodium is the principal cation in extracellular fluid. Potassium concentrations are about 30 times higher inside than outside cells, while sodium concentrations are more than 10 times lower inside than outside cells. The concentration differences between potassium and sodium across cell membranes create an electrochemical gradient known as the membrane potential.

A cell's membrane potential is maintained by ion pumps in the cell membrane, especially the sodium, potassium-ATPase pumps. These pumps use ATP (energy) to pump sodium out of the cell in exchange for potassium. Their activity has been estimated to account for 20%-40% of the resting energy expenditure in a typical adult. The large proportion of energy dedicated to maintaining sodium/potassium concentration gradients emphasizes the importance of this function in sustaining life. Tight control of cell membrane potential is critical for nerve impulse transmission, muscle contraction, and cardiac function.

Nutrient absorption and transport

Absorption of sodium in the small intestine plays an important role in the absorption of chloride, amino acids, glucose, and water. Similar mechanisms are involved in the reabsorption of these nutrients after they have been filtered from the blood by the kidneys. Chloride, in the form of hydrochloric acid (HCl), is also an important component of gastric juice, which aids the digestion and absorption of many nutrients.

Maintenance of blood volume and blood pressure

Because sodium is the primary determinant of extracellular fluid volume including blood volume, a number of physiological mechanisms that regulate blood volume and blood pressure work by adjusting the body's sodium content. In the circulatory system, pressure receptors (baroreceptors) sense changes in blood pressure and send excitatory or inhibitory signals to the nervous system and/or endocrine glands to affect sodium regulation by the kidneys. In general, sodium retention results in water retention and sodium loss results in water loss. Two of the many systems that affect blood volume and blood pressure through sodium regulation are the renin-angiotensin system and the anti-diuretic hormone (AdH) system.

Renin angiotensin-aldosterone system – In response to a significant decrease in blood volume or pressure (e.g., serious blood loss or dehydration), the kidneys release renin into the circulation. Renin is an enzyme that splits a small peptide (angiotensin I) from a larger protein (angiotensinogen) produced by the liver. Angiotensin I is split into a smaller peptide (angiotensin II) by angiotensin converting enzyme (ACE), an enzyme present on the inner surface of blood vessels, and in the lungs, liver, and kidneys. Angiotensin II stimulates the constriction of small arteries, resulting in increased blood pressure.

Angiotensin II is also a potent stimulator of aldosterone synthesis by the adrenal glands. Aldosterone is a steroid hormone that acts on the kidneys to increase the reabsorption of sodium and the excretion of potassium. Retention of sodium by the kidneys increases the retention of water, resulting in increased blood volume and blood pressure.

Anti-diuretic hormone (ADH) system – Secretion of ADH by the posterior pituitary gland is stimulated by a significant decrease in blood volume or pressure. ADH acts on the kidney to increase the reabsorption of water.

Deficiency

Sodium (and chloride) deficiency does not generally result from inadequate dietary intake, even in those on very low-salt diets. However, the use of diuretics, as well as excessive diarrhea and/or vomiting (for example in cholera), can deplete the body of sodium and chloride ions. This results in metabolic alkalosis, a condition which leads to an elevated blood pH.

Symptoms of metabolic alkalosis include decreased ventilation, a urinary pH change from alkali to acidic ranges, and excessive excretion of potassium. Hypokalemic metabolic alkalosis is an acute deficiency in potassium, accompanied by an elevation of blood and tissue pH. This disorder affects muscle function, resulting in difficult respiration and swallowing and, on occasion, death.

Toxicity

Excessive intakes of sodium chloride lead to an increase in extracellular fluid volume as water is pulled from cells to maintain normal sodium concentrations. However, as long as water needs can be met, normally functioning kidneys can excrete the excess sodium and restore the system to normal. Ingestion of large amounts of salt may lead to nausea, vomiting, diarrhea, and abdominal cramps. Abnormally high plasma sodium concentrations (hypernatremia) generally develop from excess water loss, frequently accompanied by an impaired thirst mechanism or lack of access to water. Symptoms of hypernatremia in the presence of excess fluid loss may include dizziness or fainting, low blood pressure, and diminished urine production. Severe hypernatremia may result in edema (swelling), hypertension, rapid heart rate, difficulty breathing, convulsions, coma, and death. Hypernatremia is rarely caused by excessive sodium intake (only in the ingestion of large amounts of seawater or intravenous infusion of concentrated saline solution). In end-stage renal failure (kidney failure), impaired urinary sodium excretion may lead to fluid retention, resulting in edema, high blood pressure, or congestive heart failure if salt and water intake are not restricted.

Regulation

The regulation of body sodium and body water content is well coordinated. Body osmolality is controlled by regulating the amount of water in the body through changes in thirst and renal water excretion. The regulation of osmolality dominates that of body volume. Therefore, if for some reason there is too much sodium in the body, the regulation of osmolality will cause an increase in body water content to reduce the osmolality back to normal. However, a side effect of this will be an increase in body volume. Nevertheless, a moderate change in body volume is generally better tolerated than a change in osmolality which can damage or disrupt cellular function, especially in the brain.

Body volume is regulated by changing the amount of sodium in the body. This will cause the osmolality regulating mechanisms to readjust body water content to maintain the correct osmolality by altering body volume. A gain of sodium will cause an increase in body volume and a loss of sodium will cause a reduction in body volume. In humans, the main influence on body sodium is renal sodium excretion and so renal sodium excretion is the main factor determining body volume.