Sodium ions (Na+) are necessary in small amounts for some types ofplants,[1] butsodium as a nutrient is more generally needed in larger amounts[1] byanimals, due to their use of it for generation ofnerve impulses and for maintenance ofelectrolyte balance andfluid balance. In animals, sodium ions are necessary for the aforementioned functions and forheart activity and certainmetabolic functions.[2] Thehealth effects of salt reflect what happens when the body has too much or too little sodium.Characteristic concentrations ofsodium in model organisms are: 10 mM inE. coli, 30 mM in budding yeast, 10 mM in mammalian cell and 100 mM in blood plasma.[3]
Additionally, sodium ions are essential to several cellular processes. They are responsible for the co-transport of glucose in the sodium glucose symport, are used to help maintain membrane polarity with the help of the sodium potassium pump, and are paired with water to thin the mucus of the airway lumen when the active Cystic Fibrosis Transport Receptor moves chloride ions into the airway.[4]
The minimum physiological requirement for sodium is between 115 and 500 mg per day depending on sweating due to physical activity, and whether the person is adapted to the climate.[5]Sodium chloride is the principal source of sodium in the diet, and is used as seasoning and preservative, such as forpickling andjerky; most of it comes from processed foods.[6] TheAdequate Intake for sodium is 1.2 to 1.5 g per day,[7] but on average people in the United States consume 3.4 g per day,[8][9] the minimum amount that promotes hypertension.[10] Note that salt contains about 39.3% sodium by mass[11]—the rest being chlorine and other trace chemicals; thus theTolerable Upper Intake Level of 2.3 g sodium would be about 5.9 g of salt—about 1teaspoon.[12] The average daily excretion of sodium is between 40 and 220 mEq.[13]
Normal serum sodium levels are between approximately 135 and 145mEq/L (135 to 145 mmol/L). A serum sodium level of less than 135 mEq/L qualifies ashyponatremia, which is considered severe when the serum sodium level is below 125 mEq/L.[14][15]
Therenin–angiotensin system and theatrial natriuretic peptide indirectly regulate the amount ofsignal transduction in the humancentral nervous system, which depends on sodium ion motion across the nerve cell membrane, in all nerves. Sodium is thus important inneuron function and osmoregulation between cells and theextracellular fluid; the distribution of sodium ions are mediated in all animals bysodium–potassium pumps, which are active transportersolute pumps, pumping ions against the gradient, and sodium-potassium channels.[16] Sodium channels are less selective in comparison to potassium channels. Sodium is the most prominent cation in extracellular fluid: in the 15 L ofextracellular fluid in a 70 kg human there is around 50 grams of sodium, 90% of the body's total sodium content.
Some potentneurotoxins, such asbatrachotoxin, increase the sodium ion permeability of thecell membranes in nerves and muscles, causing a massive and irreversibledepolarization of the membranes with potentially fatal consequences. However, drugs with smaller effects on sodium ion motion in nerves may have diverse pharmacological effects that range from anti-depressant to anti-seizure actions.
Since only some plants need sodium and those in small quantities, a completelyplant-based diet will generally be very low in sodium.[citation needed] This requires some herbivores to obtain their sodium fromsalt licks and other mineral sources. The animal need for sodium is probably the reason for the highly conserved ability totaste the sodium ion as "salty." Receptors for the pure salty taste respond best to sodium; otherwise, the receptors respond only to a few other small monovalent cations (Li+,NH+4 and somewhat toK+). Thecalcium 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, acting to regulateblood volume,blood pressure,osmotic equilibrium andpH.[8]
InC4 plants, sodium is amicronutrient that aids in metabolism, specifically in regeneration ofphosphoenolpyruvate (involved in the biosynthesis of various aromatic compounds, and incarbon fixation) and synthesis of chlorophyll.[17] In others, it substitutes forpotassium in several roles, such as maintainingturgor pressure and aiding in the opening and closing of stomata.[18] Excess sodium in the soil limits the uptake of water due to decreasedwater potential, which may result in wilting; similar concentrations in thecytoplasm can lead to enzyme inhibition, which in turn causes necrosis and chlorosis.[19] To avoid these problems, plants developed mechanisms that limit sodium uptake by roots, store them in cellvacuoles, and control them over long distances;[20] excess sodium may also be stored in old plant tissue, limiting the damage to new growth. Though much how excess sodium loading in the xylem is yet to be determined. However, anti porter CHX21 can be attributed to active loading of sodium into the xylem.[21]
Sodium is the primarycation (positively charged 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,[22] one of the primary ways in which the human body keeps track of loss of body water is thatosmoreceptors in thehypothalamus 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 ashypernatremia. 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 thehypothalamus, causing a decrease invasopressin hormone secretion from theposterior 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 highosmolar content.
In humans, a high-salt intake was demonstrated to attenuatenitric 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.[23]
Because thehypothalamus/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 powerfuldiuretic 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, theosmoreceptor system may sense lowered sodium concentration in the blood and then direct compensatory urinary water loss in order to correct thehyponatremic (low blood sodium) state.
Thesodium-potassium pump works with the sodium and potassium leak channels to maintain the membrane potential between the cell and the extracellular space. Sodium moves down the concentration gradient from the cytosol into the extracellular matrix. Potassium moves down its concentration gradient from the extracellular matrix into the cytosol. In order to maintain the membrane potential, the sodium-potassium pump acts as a form of direct active transport where the hydrolysis of ATP to ADP and an inorganic phosphate at the P-type ATPase moves 3 potassium ions back out of the cell and 2 sodium ions into the cell.[4]
The sodium-potassium pump plays a large role in neural signaling due to the maintenance of cell membrane potential. This creates an action potential that causes the neurons to polarize and depolarize their membranes by opening and closing the voltage gated channels: this alters voltage potential and leads to neurotransmitter secretion and ultimately signal transmission.[24]
When the pump fails to function, patients are susceptible to illnesses like heart failure and chronic obstructive lung disease (COLD). Those who experienced an event of heart failure had on average, a 40% lower concentration of the sodium-potassium ATPase. This lack of polarization of the membrane leads to an inability of action potentials to propagate at their usual rate, leading to a lowered hear rate and potentially heart failure.[25] In COLD diagnoses, a majority of patients found to have a lowered amount of magnesium and potassium also had a decreased concentration of the sodium-potassium pump in skeletal and smooth muscle during respiratory failure. COLD is treatable in the short term by glucocorticoid which up-regulates the sodium-potassium pump, helping to support muscle endurance and increase muscle activity during these episodes of respiratory failure.[26]
In thesodium-glucose symporter, sodium moves down its concentration gradient to move glucose up its concentration gradient. Sodium has a greater concentration outside of the cell, and binds to the symporter, which is in its outward facing conformation. Once sodium is bound, glucose can bind from the extracellular space, causing the symporter to switch into the occluded formation (closed) before opening to the inside of the cell and releasing the two sodium ions and the one glucose molecule. Once both are released, the symporter re-orients itself to the outward facing conformation and the process starts all over again.[4] A major example of up-regulation of the sodium-glucose symporter is seen in patients withtype 2 diabetes, where there is roughly a 3-4 fold up-regulation of the sodium-glucose symporter (SGLT1). This leads to an influx of glucose into the cell and results in hyperglycemia.[27]
TheCystic Fibrosis Transport Regulator (CFTR) works by binding two ATP to the A1 and A2, ATP-binding domain. This opens the CFTR channel and allows chloride ions to flow into the lungs and airway lumen. This influx of negatively charged chloride ions into the airway lumen causes sodium to move into the airway lumen to balance the negative charge. Water then moves in with the sodium to balance the osmotic pressure and ultimately leads to the thinning of mucus. In cases of Cystic Fibrosis, the CFTR is defective and only binds a single ATP, leading to the channel failing to open and preventing chloride ions from diffusing into the airway lumen. Since chloride ions cannot diffuse in, there is no movement of sodium into the airway lumen, and no need for water to move into the lumen, leading to thick mucus that clogs and infects the airway lumen.[4]
Thus, a minimum average requirement for adults can be estimated under conditions of maximal adaptation and without active sweating as no more than 5 mEq/day, which corresponds to 115 mg of sodium or approximately 300 mg of sodium chloride per day. In consideration of the wide variation of patterns of physical activity and climatic exposure, a safe minimum intake might be set at 500 mg/day. [Note: Table 11-1 seems to clarify that 500 mg refers to sodium, not sodium chloride]