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Medicine LibreTexts

5.5: Thirst

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  • What is thirst?

    Thirst is "the physiological urge to drink water". In studies, it is recognised when subjects report the conscious sensation of a desire to drink. Under normal conditions, most water intake is due not to thirst but to social and cultural factors (eg drinking with meals or at work breaks, water in food). Thirst offers a backup to these behavioural factors and to the ADH response. Both the thirst and the ADH mechanisms are regulated in the hypothalamus. Water intake can be considered to consist of two components: a regulatory component (due to thirst) and a non-regulatory component (all other fluid intake).

    Stimuli to Thirst

    The 4 major stimuli to thirst are:

    • Hypertonicity: Cellular dehydration acts via an osmoreceptor mechanism in the hypothalamus
    • Hypovolaemia: Low volume is sensed via the low pressure baroreceptorsin the great veins and right atrium
    • Hypotension: The high pressure baroreceptors in carotid sinus & aorta provide the sensors for this input
    • Angiotensin II: This is produced consequent to the release of renin by the kidney (eg in response to renal hypotension)

    There is strong evidence for a role of the octapeptide angiotensin II in physiological thirst: it is a potent dipsogen. The action is mediated via the effect of angiotensin II on specific receptors located in the subfornical organ (SFO) and the organum vasculosum of the lamina terminalis (OVLT). Both the SFO and the OVLT are circumventricular organs: they lie outside the blood-brain barrier allowing blood-borne substances (angiotensin II in this case) to affect neurones. The neuronal pathway from the SFO to the hypothalamus uses angiotensin II as a neurotransmitter. Ascending neural pathways arising from the low and high pressure baroreceptors enter the same area of the hypothalamus. Hypovolaemia and hypotension are facilitators for the development of thirst.

    It is not known whether the osmoreceptor which stimulates thirst is the same or different from the one stimulating ADH release but they are located in the same area of the hypothalamus. The osmotic threshold for thirst may be set higher than that for ADH release but this is disputed. If it was, it would suggest that thirst has a backup role for situations where alterations in plasma tonicity are not corrected solely by ADH changes. Thirst and ADH release are interrelated in the hypothalamus via neuronal connections between relevant areas.


    Thirst leads to drinking. This is a powerful defence against hyperosmolality. As long as access to water is unrestricted and the person is able to drink, then significant hyperosmolality will not develop. For example, elderly patients with non-ketotic hyperglycaemia do not become significantly hyperosmolar unless water intake becomes restricted for some reason.

    Drinking stimulates mechanoreceptors in the mouth and pharynx. These peripheral receptors provide input to the hypothalamus and the sensation of thirst is attenuated. This occurs even before any reduction in plasma tonicity. This may be a safeguard against over-ingestion of water as there is an inevitable delay before the ingested water is absorbed and available to decrease plasma osmolality.