The volume and tonicity of body fluids are maintained within a narrow normal range by regulation of sodium and water balance.
The volume of extracellular fluid (ECF) is determined by the total body sodium content, whereas the osmolality and sodium
concentration of ECF are determined by water balance. The kidney plays a crucial role in these processes by balancing the
excretion of salt and water with their intake and by avidly conserving them when intake is restricted.
The serum sodium concentration is an indication of the amount of sodium relative to the amount of water in the ECF and provides
no direct information about total body sodium content. Patients with hyponatremia or hypernatremia may have a decreased, normal,
or increased total body sodium content. Hypernatremia (>155 mEq/L in dogs or >162 mEq/L in cats) implies hyperosmolality,
whereas a hyponatremia (<140 mEq/L in dogs or <149 mEq/L in cats) usually, but not always, implies hyposmolality. Hyponatremia
develops when the patient is unable to excrete ingested water or when urinary and insensible fluid losses have a combined
osmolality greater than that of ingested or parenterally administered fluids. Hypernatremia develops when water intake has
been inadequate, when the lost fluid is hypotonic to extracellular fluid, or when an excessive amount of sodium has been ingested
or administered parenterally.
Extracellular fluid volume is directly dependent on body sodium content. The body is able to sense and respond to very small
changes in sodium content. The adequacy of body sodium content is perceived as the fullness of the circulating blood volume
(so-called effective circulating volume). Lowpressure mechanoreceptors (i.e., volume receptors) in the cardiac atria and pulmonary
vessels and highpressure baroreceptors (i.e., pressure receptors) in the aortic arch and carotid sinus play a primary role
in the body's ability to sense the adequacy of the circulating volume. Within the kidney, the juxtaglomerular apparatus responds
to changes in perfusion pressure with changes in renin production and release. The kidney constitutes the primary efferent
limb of sodium control and regulates sodium balance by excreting an amount of sodium each day equal to that ingested. There
are several overlapping control mechanisms for regulation of renal handling of sodium. This redundancy of controls serves
to protect against sodium imbalance should one control mechanism fail.
The osmolality of ECF and serum sodium concentration are regulated by adjusting water balance. Osmoreceptors in the hypothalamus
constitute the afferent limb (sensors) for regulation of water balance. Vasopressin (anti-diuretic hormone) release is stimulated
when the osmoreceptors shrink in response to plasma hyperosmolality and is inhibited when they swell in response to plasma
hypoosmolality. Vasopressin (water output) and thirst (water input) constitute the efferent limb (effectors) for the regulation
of water balance. Changes in plasma osmolality as small as 1 to 2% above normal lead to maximal vasopressin release. The gain
of the system is such that a 1 mOsm/kg increase in plasma osmolality leads to an almost 100 mOsm/kg increase in urine osmolality.
The vasopressin system curtails water excretion, but further defense against hypertonicity requires a normal thirst mechanism
and access to water. The next most important stimulus for vasopressin release is volume depletion sensed by baroreceptors
in the left atrium, aortic sinus, and carotid sinuses. A decrease in blood volume of 5 to 10% lowers the threshold for vasopressin
release and increases the sensitivity of the osmoregulatory mechanism. Nonosmotic stimulation of vasopressin by actual or
perceived volume depletion plays a major role in the generation and perpetuation of hyponatremia in states of true volume
depletion and in edematous states associated with hypervolemia. Other stimuli for vasopressin release include nausea, pain,
and emotional anxiety. Many drugs and some electrolyte disturbances affect the release and renal action of vasopressin. 
