Water Homeostasis and Dynamic Equilibrium

Fluid balance within the body is maintained via homeostatic mechanisms (1). The body maintains a constant state of dynamic equilibrium, fluids can shift back and forth for redistribution upon demand, but it has a strict limit on how much volume and concentration changes it will allow. The body tries to maintain the exact volume in all 3 of the interior spaces. 

Thirst and hunger drives helps the body regulate net body water balance from day-to-day. Neuroendrocrine responses, renal mechanisms and non-regulatory social behavioral factors also help regulate water balance (2).

Water is stored in the intracellular compartment (60%) and in the extracellular compartment (40%). The extracellular is subdivided into the intravascular and interstitial fluid compartments. Of those 40% of the extracellular space, 20% of the water is found in the intravascular compartment and 80% is found in the interstitial compartment.

Movement across these compartments is regulated by changes in Starling forces, which include oncotic (due to proteins) and hydrostatic pressures. In the extracellular compartment, changes in sodium concentrations alter the total extracellular fluid while plasma proteins diffuse slowly across the capillary endothelium and changes the fluid distribution: an increase in plasma proteins increases oncotic pressure and favors fluid movement into the plasma, whereas plasma protein escape increases interstitial fluid (3).

When there an acute plasma volume loss, capillary fluid dynamics or Starling forces adjust to favor plasma proteins and fluid movement out of interstitial and into vascular compartments, thereby selectively restoring plasma volume. The reason why sodium and other electrolytes are not as effective is because they freely diffuse across capillary endothelium, and this is also why sodium content is more effective at changing the total extracellular fluid (3).

The measurement of transcapillary escape of albumin from the plasma is an important indicator of the oncotic force within the plasma: a lower transcapillary escape of albumin is usually associated with an increase in plasma albumin content and plasma oncotic pressure (3).

Water (and sodium) must be constantly supplied for cardiovascular function. Plasma volume and osmolality must be maintained within set limits. This is accomplished by the release of hormones necessary to ingest and conserve water and sodium within the body.

An increased osmolality draws water from cells into the blood thus dehydrating specific brain osmoreceptors that stimulate drinking and release of anti-diuretic hormone (ADH or vasopressin). ADH reduces water loss via lowered urine volume (1).

Extracellular dehydration (hypovolaemia) stimulates specific vascular receptors that signal brain centres to initiate drinking and ADH release. Baro/volume receptors in the kidney stimulate the release of the enzyme renin that starts a cascade of events to produce angiotensin II (AngII), which initiates also drinking and ADH release (1). This stimulates also aldosterone release which reduces kidney loss of urine sodium.

Both AngII and ADH are vasoactive hormones that could work to reduce blood vessel diameter around the remaining blood. All these events work in concert so that the cardiovascular system can maintain a constant perfusion pressure, especially to the brain. Even if drinking does not take place ADH, AngII and aldosterone are still released (1).

Normal thirst mechanism with minimal drinking makes vasoconstriction permanent rather than temporary, and makes the body excrete small volumes of concentrated urine, this is why it looks darker when you are dehydrated (see Hydration: assessing hydration status).

In turn a normal hydration state with drinking makes you excrete large volume of dilute urine.

Balance in the intracellular space is critical for cell function and performance. Cells need water for organelles within them, and for thousands of metabolic reactions that occur every second. This space is very finely tuned.

The body can also shrink the intravascular space when there’s not enough blood inside the arteries, to maintain normal blood pressure. In case of dehydration (or bleeding), the vascular space can use the muscles in the vessel walls to contract, so that the total vascular space is temporarily smaller to maintain blood pressure and blood flow for some time.

Some factors influence fluid balance, for example heat and humidity. The body releases water through sweat to cool the temperature, however sweat does not evaporate when the humidity is high, so the body produces even more sweat. Low humidity is also dehydrating.

Airplane travel can also contribute to excess fluid loss, the relative humidity in the cabin gradually falls on high altitude and during prolonged flights (4), it's essentially 0% humidity in a pressurized cabin. This low humidity can cause increases in mean plasma osmolarity, mean urine osmolarity and urine specific gravidity, indicating dehydration (5). Some symptoms are the drying of the skin, mucous membranes, and dry eyes present after 3-4 hours of flight (6). However we are not losing water through sweating or exercising, but through breathing.

The kidneys play a major role in maintaining homeostasis by helping to preserve the constancy of the internal fluid. They excrete the products of bodily metabolism (waste products). Each kidney has over one million microscopic functional units known as nephrons, they are the smallest unit within the kidney enabling it to produce its functions.

The kidney have three processes involved in forming urine:

1. Glomerular filtration;
2. Tubular reabsorption;
3. Tubular secretion.


1. Thornton SN (2010). Thirst and hydration: physiology and consequences of dysfunction. Physiol Behav 100, 15–21.
2. Michael N. Sawka, PhD, Samuel N. Cheuvront, PhD, RD, and Robert Carter III, PhD, MPH. Human Water Needs. 2005 International Life Sciences Institute doi: 10.1301/nr.2005.jun.S30–S39
3. Nina S. Stachenfeld. Sex Hormone Effects on Body Fluid Regulation. Exerc Sport Sci Rev. 2008 Jul; 36(3): 152–159.
4. Sandor T. Travel thrombosis: Pathomechanisms and clinical aspects. Pathophysiology. 2008;15(4):243–52.
5. Simons R, Krol J. Jet leg, pulmonary embolism, and hypoxia. Lancet. 1996;348(9024):416.
6. Nagda NL, Hodgson M. Low relative humidity and aircraft cabin air quality. Indoor Air. 2001;11(3):200–14.