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In addition to influencing the rate of water excretion, ADH plays a central role in osmoregulation because its release is directly affected by the plasma osmolality. At a plasma osmolality of less than 275 mosm/kg, which usually represents a plasma Na + concentration of less than 135-137 mmol/L, there is essentially no circulating ADH. As the plasma osmolality rises above this threshold, however, the secretion of ADH increases progressively.
Two simple examples will illustrate the basic mechanisms of osmoregulation, which is so efficient that the plasma Na + concentration is normally maintained within 1-2% of its baseline value.
Ingestion of a water load leads to an initial reduction in the plasma osmolality, thereby diminishing the release of ADH. The ensuing reduction in water reabsorption in the collecting tubules allows the excess water to be excreted in a dilute urine.
Water loss resulting from sweating is followed by, in sequence, a rise in both plasma osmolality and ADH secretion, enhanced water reabsorption, and the appropriate excretion of a small volume of concentrated urine. This renal effect of ADH minimizes further water loss but does not replace the existing water deficit. Thus, optimal osmoregulation requires an increase in water intake, which is mediated by a concurrent stimulation of thirst. The importance of thirst can also be illustrated by studies in patients with central diabetes insipidus, who are deficient in ADH. These patients often complain of marked polyuria, which is caused by the decline in water reabsorption in the collecting tubules. However, they do not typically become hypernatraemic, because urinary water loss is offset by the thirst mechanism.
Also see Osmotic pressure, Plasma osmolality
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