Buenos Aires 01 de Febrero del 2021
BALANCE DE AGUA - REGULACION OSMOLARIDAD PLASMATICA
Water Balance and Regulation of Plasma Osmolality
Burton D. Rose, Theodore W. Post
Clinical Physiology of Acid-Base and Electrolyte Disorders
5th ed, McGraw-Hill, New York, 2001. - Chapter 9A
Hypoosmolality and hyperosmolality can produce serious neurologic symptoms and death, primarily due to water movement into and out of the brain, respectively [1-5]. To prevent this, the plasma osmolality (Posm ), which is primarily determined by the plasma Na+ concentration, is normally maintained within narrow limits by appropriate variations in water intake and water excretion. This regulatory system is governed by osmoreceptors in the hypothalamus that influence both thirst and the secretion of antidiuretic hormone (ADH).
Although it may seem that regulation of the plasma Na+ concentration must have something to do with Na+ balance, osmoregulation is almost entirely mediated by changes in water balance. Thus, the effectors for osmoregulation (ADH and thirst, affecting water excretion and water intake) are very different from those involved in volume regulation (renin-angiotensin-aldosterone system and atrial natriuretic peptide, affecting Na+ excretion) This chapter will describe the sources of water intake, the sites of water loss from the body, and the roles of ADH, thirst, and renal water excretion in the maintenance of the Posm.
Obligatory water output - In the steady state, water intake (including that generated from endogenous metabolism) must equal water output. Much of the water output involves obligatory losses in the urine, stool, and, by evaporation, from the moist surfaces of the skin and respiratory tract. The evaporative losses play an important role in thermoregulation; the heat required for evaporation, 0.58 kcal/1.0 mL of water, normally accounts for 20 to 25 percent of the heat lost from the body, with the remainder occurring by radiation and convection .
The obligatory renal water loss is directly related to solute excretion. If a subject has to excrete 800 mosmol of solute per day (mostly Na+ and K+ salts and urea) to remain in the steady state, and the maximum Uosm is 1200 mosmol/kg, then the excretion of the 800 mosmol will require a minimum urine volume of 670 mL/day.
Only small amounts of water are normally lost in the stool, averaging 100 to 200 mL/day. However, gastrointestinal losses are increased to a variable degree in patients with vomiting or diarrhea. The effect of these losses on the plasma Na+ concentration depends on the sum of the Na+ and K+ concentrations in the fluid that is lost.
Water intake - To maintain water balance, water must be taken in (or generated) to replace these losses. Net water intake is derived from three sources:
(1) ingested water
(2) water contained in foods, e.g., meat is roughly 70 percent water and certain fruits and vegetables are almost 100 percent water
(3) water produced from the oxidation of carbohydrates, proteins, and fats.
If the latter two sources account for 1200 mL/day and the obligatory water loss (from the skin, gastrointestinal tract, and in the urine) is 1600 mL/day, then at least 400 mL must be ingested by drinking to maintain balance.
Humans drink more than this minimum requirement for social and cultural reasons, and the extra water is excreted in the urine.
REGULATION OF PLASMA OSMOLALITY
The normal plasma osmolality (Posm ) is 275 to 290 mosmol/kg.
It usually is held within narrow limits as variations of only 1 to 2 percent initiate mechanisms to return the Posm to normal. These alterations in osmolality are sensed by receptor cells in the hypothalamus which affect water intake (via thirst) and water excretion (via ADH, which increases water reabsorption in the collecting tubules).
In terms of water balance, a water load decreases the Posm and water loss (as with exercise on a hot day) increases the Posm . In both of these settings, there is a parallel change in the plasma Na+ concentration.
These alterations in water balance must be differentiated from conditions of isosmotic fluid loss (such as bleeding or some cases of diarrhea), in which solute and water may be lost proportionately, producing no direct change in the Posm or the plasma Na+ concentration.
The body responds to a water load by suppressing ADH secretion, resulting in decreased collecting tubule water reabsorption and excretion of the excess water. The peak diuresis is delayed for 90 to 120 min, the time necessary for the metabolism of previously circulating ADH. As will be seen, the kidneys can excrete up to 10 to 20 liters of water per day, well above any normal level of water intake. Therefore, water retention resulting in hypoosmolality and hyponatremia occurs, with rare exceptions, only in patients with an impairment in renal water excretion.
The correction of a water deficit (hyperosmolality) requires the intake and retention of exogenous water. This is achieved by increases in thirst and ADH release, which are induced by the elevation in the Posm. In contrast to the response to hypoosmolality, in which renal water excretion is of primary importance, increased thirst is the major defense against hyperosmolality and hypernatremia. Although the kidney can minimize water excretion via the effect of ADH, a water deficit can be corrected only by increased dietary intake.
An example of the efficiency of the thirst mechanism occurs in patients with complete central diabetes insipidus who, because they secrete little or no ADH, may excrete more than 10 liters of urine per day. Despite this, the Posm remains near normal because the thirst mechanism augments water intake to match output. Thus, symptomatic hypernatremia generally will not occur in a patient with a normal thirst mechanism and access to water..
Excretion of a water load generally occurs so rapidly that there is little change in volume and no activation of the volume regulatory pathways. There are, however, settings in which both the volume and osmoregulatory systems come into play. As an example, the intake of NaCl without water (as with a large quantity of potato chips) results in an elevation in the Posm and, due to the rise in extracellular Na+ stores, expansion of the effective circulating volume. The latter change promotes the renal excretion of the excess Na+, via a response that is mediated at least in part by a reduction in the release of aldosterone and an increase in that of atrial natriuretic peptide. ADH secretion and thirst also are stimulated (by the rise in Posm); the ensuing increment in water intake both lowers the Posm toward normal and further expands the volume, thereby enhancing the stimulus to renal Na+ excretion. The end result is that the urine has a high osmolality and a relatively high concentration of Na+, a composition that is similar to net intake.
In comparison, an infusion of isotonic saline causes volume expansion, but does not change the Posm. Consequently, ADH release and thirst are not directly affected, and the steady state is restored by the volume regulatory pathways.
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