Water and sodium balance

Body water and the electrolytes it con- tains are in a state of constant flux. We drink, we eat, we pass urine and we sweat; during all this it is important that we maintain a steady state. A motor car’s petrol tank might hold about 42 L, similar to the total body water content of the average 70 kg male. If 2 L were lost quickly from the tank it would hardly register on the fuel indicator. However, if we were to lose the same volume from our intravascular compart- ment we would be in serious trouble. We are vulnerable to changes in our fluid compartments, and a number of important homeostatic mechanisms exist to prevent or minimize these. Changes to the electrolyte concentration are also kept to a minimum. 

To survive, multicellular organisms must maintain their ECF volume. Humans deprived of fluids die after a few days from circulatory collapse as a result of the reduction in the total body water. Failure to maintain ECF volume, with the consequence of impaired blood circulation, rapidly leads to tissue death due to lack of oxygen and nutrients, and failure to remove waste products.

Water 

Normal water balance is illustrated in Figure 7.1.

Water intake largely depends on social habits and is very variable. Some people drink less than half a litre each day, and others may imbibe more than 5 L in 24 hours without harm. Thirst is rarely an overriding factor in determining intake in Western societies.

Fig 7.1 Normal water balance.

Water losses are equally variable and are normally seen as changes in the volume of urine produced. The kidneys can respond quickly to meet the body’s need to get rid of water. The urine flow rate can vary widely in a very short time. However, even when there is need to conserve water, man cannot completely shut down urine production. Total body water remains remarkably constant in health despite massive fluctuations in intake. Water excretion by the kidney is very tightly controlled by arginine vaso- pressin (AVP; also called antidiuretic hormone, ADH). 

The body is also continually losing water through the skin as perspiration, and from the lungs during respiration. This is called the ‘insensible’ loss. This water loss amounts to between 500 and 850 mL/day. Water may also be lost in disease from fistulae, or in diarrhoea, or because of prolonged vomiting. 

AVP and the regulation of osmolality 

Specialized cells in the hypothalamus sense differences between their intracellular osmolality and that of the extracellular fluid, and adjust the secretion of AVP from the posterior pituitary gland. A rising osmolality promotes the secretion of AVP while a declining osmolality switches the secretion off (Fig 7.2). AVP causes water to be retained by the kidneys. Fluid deprivation results in the stimulation of endogenous AVP secretion, which reduces the urine flow rate to as little as 0.5 mL/minute in order to conserve body water. However, within an hour of drinking 2 L of water, the

Fig 7.2 The regulation  of water balance by AVP and osmolality.

urine flow rate may rise to 15 mL/ minute as AVP secretion is shut down. Thus, by regulating water excretion or retention, AVP maintains normal elec- trolyte concentrations within the body. 

Sodium 

The total body sodium of the average 70 kg man is approximately 3700 mmol, of which approximately 75% is exchange- able (Fig 7.3). A quarter of the body sodium is termed non-exchangeable, which means it is incoporated into tissues such as bone and has a slow turnover rate. Most of the exchangeable sodium is in the extracellular fluid. In the ECF, which comprises both the plasma and the interstitial fluid, the sodium concentration is tightly regulated at around 140 mmol/L. 

Sodium intake is variable, a range of less than 100 mmoL/day to more than 300 mmol/day being encountered in Western societies. In health, total body sodium does not change even if intake falls to as little as 5 mmol/day or is greater than 750 mmol/day. 

Sodium losses are just as variable. In practical terms, urinary sodium excre- tion matches sodium intake. Most sodium excretion is via the kidneys. Some sodium is lost in sweat (approxi- mately 5 mmol/day) and in the faeces (approximately 5 mmol/day). In disease the gastrointestinal tract is often the major route of sodium loss. This is a very important clinical point, especially in paediatric practice, as infantile diar- rhoea may result in death from salt and water depletion.

Fig 7.3 Normal sodium balance.

Urinary sodium output is regulated by two hormones: 

- aldosterone 

- atrial natriuretic peptide. 

Aldosterone Aldosterone decreases urinary sodium excretion by increasing sodium reabsorption in the renal tubules at the expense of potassium and hydrogen ions. Aldosterone also stimulates sodium conservation by the sweat glands and the mucosal cells of the colon, but in normal circumstances these effects are trivial. A major stimulus to aldosterone secretion is the volume of the ECF. Specialized cells in the juxtaglomerular apparatus of the nephron sense decreases in blood pressure and secrete renin, the first step in a sequence of events that leads to the secretion of aldosterone by the glomerular zone of the adrenal cortex (Fig 7.4). 

Atrial natriuretic peptide 

Atrial natriuretic peptide is a polypep- tide hormone predominantly secreted by the cardiocytes of the right atrium of the heart. It increases urinary sodium excretion. The physiological role, if any, of this hormone is unclear, but it probably plays a role in the regulation of ECF volume and sodium balance. To date, no disease state can be attributed to a primary disorder in the secretion of atrial natriuretic peptide. 

Regulation of volume 

It is important to realize that water will only remain in the extracellular 

Fig 7.4 The regulation  of sodium balance by aldosterone.

compartment if it is held there by the osmotic effect of ions. As sodium (and accompanying anions, mainly chloride) are largely restricted to the extracellular compartment, the amount of sodium in the ECF determines what the volume of the compartment will be. This is an important concept. Aldosterone and AVP interact to maintain normal volume and concentration of the ECF. Consider a patient who has been vomiting and has diarrhoea from a gastrointestinal infection. With no intake the patient becomes fluid depleted. Water and sodium have been lost. Because the ECF volume is low, aldosterone secretion is high. Thus, as the patient begins to take fluids orally, any salt ingested is maximally retained. As this raises the ECF osmolality, AVP action then ensures that water is retained too. Thus, aldosterone and AVP interac- tion continues until ECF fluid volume and composition return to normal.

Clinical note 

Assessment of the volumes of body fluid compartments is not carried out in the clinical biochemistry laboratory. This must be done clinically by history taking and examination.

Water and sodium balance

- Water is lost from the body as urine and as obligatory ‘insensible’ losses from the skin and lungs.

- Sodium may be lost from the body in urine or from the gut, e.g. prolonged vomiting, diarrhoea and intestinal fistulae.

- Arginine vasopressin (AVP) regulates renal water loss and thus causes changes in the osmolality of body fluid compartments.

- Aldosterone regulates renal sodium loss and controls the sodium content of the ECF.

- Changes in sodium content of the ECF cause changes in volume of this compartment because of the combined actions of AVP and aldosterone.