Part of “CHAPTER 25 – PHYSIOLOGY OF VASOPRESSIN, OXYTOCIN, AND THIRST“

The thirst mechanism provides an indispensable adjunct to the antidiuretic control of water balance in humans (see Chap. 26 and Chap. 27). Thirst is stimulated by many of the same variables that cause vasopressin release,53 the most potent of which appears to be hypertonicity. In healthy adults, a rise in effective plasma osmolality to 2% to 3% above basal levels produces a strong desire to drink. The absolute level of plasma osmolality at which a desire for water is first perceived may be termed the osmotic threshold for thirst. This threshold varies appreciably, but among healthy adults, it averages ˜295 mOsm/kg (see Fig. 25-4). This level is higher than the osmotic threshold for vasopressin release and closely approximates the level at which the amount of hormone secreted is sufficient to produce maximal concentration of the urine (see Fig. 25-5). The osmoreceptors that regulate thirst appear to be located in the anterolateral hypothalamus near, but not totally coincident with, those responsible for vasopressin release.54 The sensitivity and solute specificity of the thirst and vasopressin osmoreceptors also appear to be similar. Thus, the intensity of thirst and the amount of water ingested increase rapidly in direct proportion to plasma sodium or osmolality. As with vasopressin secretion, thirst is not stimulated in healthy adults when the rise in plasma osmolality is secondary to urea or glucose. However, thirst, as well as vasopressin release, is stimulated by hypergly-cemia in insulin-deficient diabetics, probably because insulin is necessary for uptake of glucose by both types of osmoreceptor.