Electrolytes, such as potassium, sodium, and chloride work to form concentration and charge differences across cell membranes, facilitating the movement of molecules in and out of the cell. Fluid inside the cell (known as intracellular fluid) has a high concentration of potassium ions and a low concentration of sodium and chloride ions. Fluid outside the cell (known as extracellular fluid (ECF)), has a comparatively low concentration of potassium ions and a high concentration of sodium and chloride ions. The compartmentalisation of these ions is maintained by their relative polarity, with choride acting as the counter anion (-ve) to potassium and sodium cations (+ve).
Regulation of the sodium content in the ECF is closely related to the body's control of ECF volume and thus water balance and blood pressure. Increasing sodium concentration in the ECF results in the retention of water and a coresponding rise in ECF volume. Conversely, a decreasing sodium concentration signals an increase in the excretion of water and a corresponding fall in ECF volume.
These changes to ECF volume are mediated by pressure receptors in the circulatory system which send excitatory or inhibitory signals to the nervous system and/or endocrine glands to instruct sodium regulation by the kidneys. Decreases to ECF volume or blood pressure are countered by release from the kidney of the enzyme renin, which helps to form the peptide angiotensin II, which in turn facilitates production of the steroid hormone aldosterone. Angiotensin II acts to constrict arterioles and thus raise blood pressure, while aldosterone stimulates the reabsorption of sodium and the excretion of potassium by the kidneys, thereby increasing the retention of water. In tandem, increased secretion of anti-diuretic hormone (ADH) by the pituitary gland causes the kidneys to increase the reabsorption of water and decrease the production of urine.