Sodium ions

Sodium ions (often referred to as just "sodium") are necessary for regulation of blood and body fluids, transmission of nerve impulses, heart activity, and certain metabolic functions. Interestingly, although sodium is needed by animals, which maintain a high blood sodium concentration and extracellular fluid sodium concentration, the ion is not needed by plants, and is generally phytotoxic. A completely plant-based diet, therefore, will be very low in sodium. This requires some herbivores to obtain their sodium from salt licks and other mineral sources. The animal need for sodium is probably the reason for the highly-conserved ability to taste the sodium ion as "salty." Receptors for the pure salty taste respond best to sodium, otherwise only to a few other small monovalent cations (Li+, NH4+, and somewhat to K+). Calcium ion (Ca2+) also tastes salty and sometimes bitter to some people but like potassium, can trigger other tastes.

Sodium ions play a diverse and important role in many physiological processes. Excitable animal cells, for example, rely on the entry of Na+ to cause a depolarization. An example of this is signal transduction in the human central nervous system, which depends on sodium ion motion across the nerve cell membrane, in all nerves.

Some potent neurotoxins, such as batrachotoxin, increase the sodium ion permeability of the cell membranes in nerves and muscles, causing a massive and irreversible depolarization of the membranes, with potentially fatal consequences. However, drugs with smaller effects on sodium ion motion in nerves may have diverse pharmacological effects which range from anti-depressant to anti-seizure actions.

Sodium is the primary cation (positive ion) in extracellular fluids in animals and humans. These fluids, such as blood plasma and extracellular fluids in other tissues, bathe cells and carry out transport functions for nutrients and wastes. Sodium is also the principal cation in seawater, although the concentration there is about 3.8 times what it is normally in extracellular body fluids.

Although the system for maintaining optimal salt and water balance in the body is a complex one, one of the primary ways in which the human body keeps track of loss of body water is that osmoreceptors in the hypothalamus sense a balance of sodium and water concentration in extracellular fluids. Relative loss of body water will cause sodium concentration to rise higher than normal, a condition known as hypernatremia. This ordinarily results in thirst. Conversely, an excess of body water caused by drinking will result in too little sodium in the blood (hyponatremia), a condition which is again sensed by the hypothalamus, causing a decrease in vasopressin hormone secretion from the posterior pituitary, and a consequent loss of water in the urine, which acts to restore blood sodium concentrations to normal.

Severely dehydrated persons, such as people rescued from ocean or desert survival situations, usually have very high blood sodium concentrations. These must be very carefully and slowly returned to normal, since too-rapid correction of hypernatremia may result in brain damage from cellular swelling, as water moves suddenly into cells with high osmolar content.

Because the hypothalamus/osmoreceptor system ordinarily works well to cause drinking or urination to restore the body's sodium concentrations to normal, this system can be used in medical treatment to regulate the body's total fluid content, by first controlling the body's sodium content. Thus, when a powerful diuretic drug is given which causes the kidneys to excrete sodium, the effect is accompanied by an excretion of body water (water loss accompanies sodium loss). This happens because the kidney is unable to efficiently retain water while excreting large amounts of sodium. In addition, after sodium excretion, the osmoreceptor system may sense lowered sodium concentration in the blood and then direct compensatory urinary water loss in order to correct the hyponatremic (low blood sodium) state.

In humans, a high-salt intake was demonstrated to attenuate nitric oxide production. Nitric oxide (NO) contributes to vessel homeostasis by inhibiting vascular smooth muscle contraction and growth, platelet aggregation, and leukocyte adhesion to the endothelium