Sodium is an important cation distributed primarily outside the cell . The cell sodium concentration is about 15 mmol/l but varies in different organs and with an intracellular volume of 30 litres about 400 mmol are inside the cell. The plasma and interstitial sodium is about 140 mmol/l with an extracellular volume of about 13 litres, 1,800 mmol are in the extracellular space. The total body sodium, however, is about 3,700 mmol as there is about 1,500 mmol stored in bones.
The body has potent sodium retaining mechanisms and even if a person is on five mmol Na+/day they can maintain sodium balance. Extra sodium is lost from the body by reducing the activity of the renin-angiotensin-aldosterone system which leads to increased sodium loss from the body. Sodium is lost through the kidneys, sweat, and feces.
In states of sodium depletion aldosterone levels increase. In states of sodium excess aldosterone levels decrease. The major physiological controller of aldosterone secretion is the plasma angiotensin II level which increases aldosterone secretion. A high plasma potassium also increases aldosterone secretion because besides retaining Na+ high plasma aldosterone causes K+ loss by the kidney. Plasma Na+ levels have little effect on aldosterone secretion.
Renin-angiotensin-aldosterone system
Regulation of sodium via the hormones renin, angiotensin, and aldosterone. In states of sodium depletion, aldosterone levels increase, and in states of sodium excess, aldosterone levels decrease.
A low renal perfusion pressure stimulates the release of renin, which forms angiotensin I which is converted to angiotensin II. Angiotensin II will correct the low perfusion pressure by causing constriction of blood vessels and by increasing sodium retention by a direct effect on the proximal renal tubule and by an effect operated through aldosterone. The perfusion pressure to the adrenal gland has little direct effect on aldosterone secretion and the low blood pressure operates to control aldosterone via the renin angiotensin system. Aldosterone also acts on the sweat ducts and colonic epithelium to conserve sodium. When aldosterone has been activated to retain sodium the plasma sodium tends to rise. This immediately causes release of ADH which causes water to be retained, thus retaining Na+ and H2O in the right proportion to restore plasma volume.
In addition to aldosterone and angiotensin II other factors influence sodium excretion. Atrial peptide also causes loss of sodium by the kidneys: it is secreted from the heart in high sodium states due either to excess intake or cardiac disease. Elevated blood pressure will also tend to cause Na+ loss and a low blood pressure usually leads to sodium retention.