Water homeostasis – Total body water (TBW) contributes to 78% of body weight at birth, but declines rapidly due to physiological diuresis in newborns and growth of low-water adipose tissue in late infancy, to reach the adult level of —55-60% by one year of age.

Post-pubertal females and obese persons have relatively less body water due to excess fat accumulation. In non-obese children, TBW or water homeostasis may be calculated as —

TBW (liters) = 0.61 x Body weight in kg + 0.251.

TBW is distributed into four body compartments a) Extracellular compartment or ECF (20-25%) as plasma (5%) and interstitial fluid (15%), b) intracellular compartment or ICF (30-40%), c) Transcellular water (2%) as urine, gut secretions, CSF and body cavity fluids, and d) Slowly exchangeable fluid compartment in bones, cartilages and connective tissue.

At birth, ECF is more than ICF, but this ratio is reversed by the end of infancy due to postnatal diuresis and cellular growth. Transcellular water and water in slowly exchangeable fluid compartments, though important metabolically, does not play significant role in water homeostasis.

Water homeostasis may be broadly divided into overall quantitative regulation of TBW and its inter-compartmental distribution, as follows —

A) TBW water homeostasis revolves around the maintenance of normal plasma volume and osmolality.

Volume of the TBW depends on the equilibrium between external intake + endogenous production* on one side and excretion via urine (65%), skin (40%); lungs (15%) and stools (5%) on other side. (*Small amount of water is produced endogenously on oxidation of nutrients).

Water homeostasis

Water homeostasis of the plasma depends on the pressure exerted by its two components a) Colloids e.g. albumin, and b) Crystalloids or electrolytes e.g. Na and Cl-. Though colloidal (oncotic) pressure contributes only to a small fraction of total plasma osmotic pressure, it is more important determinant of water homeostasis gradient across the cell membranes than crystalloid pressure, as colloids do not pass through cell membranes. (285-295 mOsm/kg 1120).

Normal plasma water homeostasis in kg roughly equals to the twice of plasma sodium concentration in meq/L, though may be precisely calculated by following formula —

Glucose BUN

Osmolahty = 2 (Na + K) + 18 + 18

Osmolality in mOsm/kg; Na/K in meqiL; Glucose/BUN in mg/dl.

Important regulatory mechanisms for TRW water homeostasis balance in human body are as follows

a) water homeostasis or Water intake depends on thirst i.e. conscious desire to drink water, which is regulated by a center in mid- hypothalamus, via two important afferents – osmoreceptors in hypothalamus to detect changes in plasma osmolality and baroreceptors in atria & vascular bed to sense changes in plasma volume. Probably, elevated Angiotensin II levels in hypovolemic states also stimulate thirst.

Primary disorders of thirst i.e. polydipsia or adipsia are usually psychogenic in origin, though altered thirst may also indicate hypothalamic disorders, hypokalemia, malnutrition and disorders of Renin-Angiotensin system.

b) Urinary excretion is the most important determinant of TBW water homeostasis regulation. A part of urinary water excretion is obligatory, necessary to excrete the solute load. However beyond this, urinary volume is regulated by a) plasma volume & osmolality, b) dietary solute load, c) renal functions, and d) hormonal control. Three important hormonal regulators of urinary water excretion are Antidiuretic hormone (ADH), aldosterone and atrial natriuretic hormone.

• Antidiuretic honnone of hypothalamic-hypophyseal axis, is a direct regulator of urinary water excretion. Its secretion is regulated by osmotic pressure of ECF and it acts by increasing the cell-permeability of collecting ducts to enhance water absorption.

Important water homeostasis disorders include

a) excess secretion in neurological disorders i.e. Syndrome of inappropriate secretion or SIADH,

b) ADH deficiency in central diabetes insipidus, and

c) Tubular non-responsiveness to ADH in Nephrogenic diabetes insipidus.

• Aldosterone – an adrenal hormone, is an indirect regulator of urinary water excretion, by manipulating sodium excretion. It is mainly secreted in response to reduced plasma volume via Renin-Angiotensin mechanism and increases tubular sodium re absorption with passive water absorption.

• Atrial natriuretic hormone is produced and stored in atrial myocytes and released in response to ECF overload leading to atrial stretching. It prevents the sodium/water re absorption by antagonizing the Renin-Angiotensin mechanism water homeostasis.

c) Non-urinary losses in stools or insensible losses via skin/lungs are fairly constant in normal children with little influence on overall water balance. However, these are important exits in pathological states e.g. diarrhea (stools), fever (skin), respiratory distress (lungs). Insensible losses are also influenced by environmental temperature, humidity and body surface area, which should be considered during calculation of fluid requirements in sick children.

B) Inter-compartmental distribution: Water in ECF and ICF compartments is freely exchangeable and exists in a state of dynamic equilibrium. Within ECF too, water continuously moves between plasma to interstitial fluids. Important determinants of these inter-compartmental water homeostasis are as follows —

Extracellular vs. Intracellular Fluid: water homeostasis between these two compartments depends on the relative osmotic gradient and active movement of ions.

While sodium is the principle cation in ECF, potassium is principle cation in ICF. As cell membranes are free permeable to water, osmotic force across them is maintained by active transport of Na out of the cell (and K into the cell) – an energy-consuming process. Any change in Na content of ECF alters its osmolality with secondary effects in ICF.

For example, hypernatremia increases osmolality of ECF> movement of water from ICF to ECF > cellular dehydration. Conversely, hyponatremia leads to movement of water into the cell and consequent cellular edema.

Plasma vs. Interstitial fluid: Interstitial fluid is derived from plasma, filtered through the semi-permeable capillary bed at the arteriolar end. However, most of it returns back to plasma at venular end, while the rest is carried back to vascular space via lymphatics. Important determinant of fluid movements or water homeostasis between plasma and interstitial are —

a) Hydrostatic pressure in capillary bed that facilitates water movement from plasma to interstitial space.

b) Osmotic pressure of plasma that prevents or reverts this movement; and

c) Capillary permeability.

In normal conditions, water homeostasis gradient between plasma & interstitial space (28 – 4.5 = 23.5 mmHg) and capillary permeability is virtually constant, and water movement between these compartments is mainly decided by hydrostatic pressure, as follows —

• At the arteriolar end of capillary bed, hydrostatic pressure is more in vascular space than in interstitial space. Consequently, net hydrostatic pressure gradient (25 — (-7) = 32 mmHg) exceeds osmotic gradient (23.5 mmllg) and water moves out into interstitial spaces.

• At venular end, hydrostatic pressure in vascular space drops to 9 mm Hg. Consequently, net pressure gradient (9 — (-7) = 16 mmHg) is less than osmotic gradient and water moves back in vascular space. Some interstitial fluid is collected by lymphatics to retum in vascular compartment (water homeostasis).

Check the below video on Water Homeostasis mechanism –