Regulation of ECF Sodium

In a mature, nonpregnant, nonlactating, healthy animal, sodium excretion matches sodium intake and is often used to estimate it, although this is not reliable, especially when intake is low. Dietary sodium is readily available, i.e., readily absorbed; thus the traditional view of sodium regulation emphasizes renal regulation of urinary Na+ loss. This oversimplifies the more subtle interplay seen, for example, in herbivorous animals, where salt appetite may contribute to regulation by intensifying during sodium depletion. Moreover, in many herbivores the feces, rather than urine, may be the major route of sodium excretion and the gut may therefore be an important regulator of sodium balance. Indeed, it is interesting that sodium transport mechanisms in the small intestine show considerable similarities to those of the proximal part of the renal tubules (e.g., linked transport of Na+, glucose, and amino acids) whereas the colon, like the distal nephron, responds to the salt-retaining (and potassium-shedding) hormone of the adrenal cortex, aldosterone. Indeed, diarrhea is essentially enteric diuresis; a failure of intestinal sodium and water reabsorbtion, which exceeds the compensatory capacity of the color.

Provided that the adrenal gland is healthy, urinary and fecal sodium loss can be reduced virtually to zero. Sweat loss can also be very low, although with severe exertion in hot climates the volume of sweat may exceed the ability of aldosterone to reduce its sodium concentration and net loss of sodium can occur. Aldosterone also reduces salivary sodium (and raises [K+]).

There are two components to the regulation of ECF sodium: the total amount of sodium retained and its concentration. The former is regulated by mechanisms that directly affect sodium, whereas the latter is essentially regulated via water balance. Thus, whatever sodium is retained in ECF is 'clothed' with the appropriate amount of water to maintain the normal plasma sodium concentration within narrow limits; deviations of less than 1% (hard to measure in the laboratory) trigger corrective responses. Thus, a raised plasma sodium concentration (e.g., after water loss) stimulates both thirst and renal water conservation; antidiuretic hormone (ADH) from the posterior pituitary reduces urine output through its effect on the renal collecting ducts. Even one of these mechanisms can defend body water; thus diabetes insipidus (inadequate production or effect of ADH) does not cause severe dehydration but polydipsia (increased fluid intake; 'thirst' is a sensation).

Excess salt intake does not raise plasma sodium concentration (hypernatremia) if water is available and the patient can drink; the excess sodium is diluted. The resulting increase in ECF volume then stimulates increased sodium excretion. Sodium also enables ECF to hold water against the osmotic 'pull' of the solutes in ICF and sodium thus functions as the 'osmotic skeleton' of ECF; it is the main determinant of its volume.

Plasma sodium concentration is therefore only indirectly related to sodium balance. When ECF volume, notably circulating volume, is severely reduced, this stimulus, rather than Na+ concentration, becomes the main drive for thirst and ADH secretion. Until ECF volume is restored, water is retained (to protect ECF volume) even though this undermines the protection of ECF Na+ concentration and, as a result, plasma sodium falls. Thus, during sodium depletion, contraction of ECF volume precedes significant reductions of plasma Na+, which is therefore a poor index of sodium status.

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