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Sodium is an essential element for all animals and some plants. Sodium ions are the major cation in the extracellular fluid (ECF) and as such are the major contributor to the ECF osmotic pressure and ECF compartment volume. Loss of water from the ECF compartment increases the sodium concentration, a condition called hypernatremia. Isotonic loss of water and sodium from the ECF compartment decreases the size of that compartment in a condition called ECF hypovolemia. By means of the sodium-potassium pump, living human cells pump three sodium ions out of the cell in exchange for two potassium ions pumped in; comparing ion concentrations across the cell membrane, inside to outside, potassium measures about 40:1, and sodium, about 1:10. In nerve cells, the electrical charge across the cell membrane enables transmission of the nerve impulse—an action potential—when the charge is dissipated; sodium plays a key role in that activity.
In humans, sodium is an essential mineral that regulates blood volume, blood pressure, osmotic equilibrium and pH; the minimum physiological requirement for sodium is 500 milligrams per day. Sodium chloride is the principal source of sodium in the diet, and is used as seasoning and preservative in such commodities as pickled preserves and jerky; for Americans, most sodium chloride comes from processed foods. Other sources of sodium are its natural occurrence in food and such food additives as monosodium glutamate (MSG), sodium nitrite, sodium saccharin, baking soda (sodium bicarbonate), and sodium benzoate. The US Institute of Medicine set its Tolerable Upper Intake Level for sodium at 2.3 grams per day, but the average person in the United States consumes 3.4 grams per day. Studies have found that lowering sodium intake by 2 g per day tends to lower systolic blood pressure by about two to four mm Hg. It has been estimated that such a decrease in sodium intake would lead to between 9 and 17% fewer cases of hypertension.
Hypertension causes 7.6 million premature deaths worldwide each year. (Note that salt contains about 39.3% sodium—the rest being chlorine and trace chemicals; thus, 2.3 g sodium is about 5.9 g, or 2.7 ml of salt—about half a US teaspoon.) The American Heart Association recommends no more than 1.5 g of sodium per day.
One study found that people with or without hypertension who excreted less than 3 grams of sodium per day in their urine (and therefore were taking in less than 3 g/d) had a higher risk of death, stroke, or heart attack than those excreting 4 to 5 grams per day. Levels of 7 g per day or more in people with hypertension were associated with higher mortality and cardiovascular events, but this was not found to be true for people without hypertension. The US FDA states that adults with hypertension and prehypertension should reduce daily intake to 1.5 g.
The renin-angiotensin system regulates the amount of fluid and sodium concentration in the body. Reduction of blood pressure and sodium concentration in the kidney result in the production of renin, which in turn produces aldosterone and angiotensin, retaining sodium in the urine. When the concentration of sodium increases, the production of renin decreases, and the sodium concentration returns to normal. The sodium ion (Na+) is an important electrolyte in neuron function, and in osmoregulation between cells and the extracellular fluid. This is accomplished in all animals by Na+/K+-ATPase, an active transporter pumping ions against the gradient, and sodium/potassium channels. Sodium is the most prevalent metallic ion in extracellular fluid.
Unusually low or high sodium levels in humans are recognized in medicine as hyponatremia and hypernatremia. These conditions may be caused by genetic factors, ageing, or prolonged vomiting or diarrhea.
In C4 plants, sodium is a micronutrient that aids in metabolism, specifically in regeneration of phosphoenolpyruvate and synthesis of chlorophyll. In others, it substitutes for potassium in several roles, such as maintaining turgor pressure and aiding in the opening and closing of stomata. Excess sodium in the soil limits the uptake of water by decreasing the water potential, which may result in plant wilting; excess concentrations in the cytoplasm can lead to enzyme inhibition, which in turn causes necrosis and chlorosis. In response, some plants developed mechanisms to limit sodium uptake in the roots, to store it in cell vacuoles, and restriction of salt transport from roots to leaves; excess sodium may also be stored in old plant tissue, limiting the damage to new growth.