Thirst and Water‐Salt Appetite

Abstract

In this chapter, the current theoretical concepts and known physiological mechanisms for mammalian fluid homeostasis are reviewed. Fluid loss from the intracellular fluid compartment is sensed by osmoreceptors, which are located peripherally in structures such as the liver as well as in the brain, and underlie osmotic or intracellular thirst and water intake. Fluid loss from the extracellular fluid compartment is sensed by pressure‐sensitive cardiopulmonary receptors, and underlies hypovolemic or extracellular thirst and water intake. The peptide hormone, angiotensin II, released during hypovolemia may contribute to extracellular thirst. Both types of dehydration produce vasopressin secretion; its primary role is to minimize further fluid loss from the kidney and it does not seem to contribute to thirst. Brain structures of the forebrain lamina terminalis are critically involved in transduction and integration of this neurosensory and hormonal information to engage drinking behavior, for example naturally‐occurring thirst such as after deprivation or during meals. Aspects of thirst during ontogeny and aging, as well as genetic and individual differences in thirst are discussed briefly. Extracellular dehydration involves loss of sodium as well as water, and so both preference and appetite for sodium, and the roles of the hormones aldosterone and angiotensin II are reviewed. Several problem areas in which our knowledge is less complete are also identified.