salt

salt has always been an important commodity, especially in hot climates, where salt loss through the sweat can be considerable. Soldiers of the Roman legions were often paid part of their stipend in salt — the so-called salerium argentinium, giving us the word salary.

Salts in general are formed, together with water, when acids react with bases, but the common meaning of ‘salt’ refers in particular to sodium chloride, the same material that is found in salt cellars. Normal saline is a solution of salt in pure water containing 0.9 g of sodium chloride per 100 ml. This solution is often used for bathing and cleaning wounds, or given by intravenous infusion after excessive blood loss — but why is it called ‘normal’? It is because the solution has the same tonicity as blood. Tonicity is a term related to osmotic strength, a property determined by the total number of molecules or ions in a given volume of solution. If living cells are bathed in a hypertonic saline (with a greater tonicity than normal saline) then the cells shrink and cease to function properly, as water passes outwards from the cells into the concentrated solution. Conversely, if living cells are bathed in hypotonic saline (lower tonicity than normal saline) they swell, water passing from the dilute solution into the cells, and eventually the cells may burst. Thus fluids that exist in different body compartments must be of the same tonicity, to avoid any such shrinkage or swelling. Salt — that is, sodium chloride — is one of the most important salts used by the body to keep fluids at their correct osmotic strength.

In a 70 kg person, the extracellular fluid contains an amount of sodium ions equivalent to 125 g of salt, while in the intracellular fluid — the sum total inside all body cells — there is the equivalent of 25 g of salt. With an average urine output of 1 litre per day there is a loss of about 9 g of salt per day. The kidneys filter off from the blood the equivalent of around 1500 g/day of salt, of which 99.5% is reabsorbed as the filtrate passes down the kidney tubules, so that only 0.5% ends up in the urine. There are also small losses of salt in the saliva and faeces, and during strenuous exertion — particularly in a hot environment — there is significant salt loss through the sweat. Clearly the salt loss must be made up by dietary intake, but this alone is not sufficiently precise to keep the tonicity of body fluids constant. Therefore the body has control mechanisms to regulate salt levels, by either increasing or reducing its excretion. If the intake of salt is insufficient, keeping the concentration correct causes the extracellular fluid volume to decrease, with consequent dehydration.

As with most bodily control mechanisms, there is a system for dealing with deficiency as well as one for dealing with excess. They are, respectively, the renin-angiotensin system and atrial natriuretic peptide.

When the body is short of salt the extracellular fluid volume, including the circulating blood volume, decreases, and the blood pressure may fall; the sodium concentration falls and the potassium ion concentration may rise, especially in those eating a low sodium diet. All these changes act directly or indirectly as stimuli for the release of the enzyme renin in the kidneys, triggering a sequence of chemical events in the blood of which the end product is angiotensin II. This is a powerful constrictor of blood vessels and therefore counteracts any fall in blood pressure. Many people with hypertension are treated with drugs which block the enzyme required for angiotensin II formation. (This same converting enzyme also breaks down kinins, which are powerful vasodilators, and therefore tend to lower the blood pressure. When kinins are preserved by inhibiting the converting enzyme, the decrease in blood pressure is probably due to both a lack of angiotensin II and also an excess of kinins.)

Angiotensin II also acts on the adrenal cortex to liberate aldosterone, which in turn causes the kidneys to increase the reabsorption of sodium ions from the filtered fluid.

When salt intake is excessive, the extracellular fluid volume and the blood pressure rise; stretching of the atria of the heart causes the release of stored granules that contain atrial natriuretic peptide. As the name implies (natrium; sodium: ouron; urine) this peptide causes natriuresis; that is, it acts on the kidneys to increase salt loss in the urine by reducing its reabsorption. More water is lost along with the salt, so the excess fluid volume is corrected.

In man excess salt intake has been considered to cause hypertension, but the supporting evidence is equivocal. Certainly there are salt-sensitive strains of laboratory animals that become hypertensive when fed salt, but other strains do not. In the animal kingdom low salt content of the diet is a problem. In seed-eating birds, like parrots, the seeds contain very little salt and an avid salt retaining mechanism has developed in the terminal part of the gut, the coprodaeum, so that little or no salt is lost in the faeces. Similarly, in frogs and toads, salt is avidly reabsorbed from the bladder, so that urine is free of salt. Darwin described how some primitive peoples would pick up a large toad (Bufo marinus), gently squeeze it, and be rewarded with several fluid ounces of almost pure water.

The old medical name, from the time when prescriptions were written in Latin to prevent patients knowing what they were getting, is nat. mur., standing for natrium of muriate. Muriatic acid is hydrochloric acid, therefore nat. mur. is the chloride salt of natrium — that is, sodium. Many popular homeopathic remedies of today contain nat. mur. in infinitesimally low amounts. The reader may ponder how adding such miniscule amounts of salt to the very large quantities already present in the body can have any effect whatsoever.

Alan W. Cuthbert

See also blood pressure; body fluids; kidneys; sweating; water balance.