Thirst

Abstract

Our bodies are mostly water, and this water is constantly being lost through evaporative and other means. Thus the evolution of robust mechanisms for finding and consuming water has been critical for the survival of most animals. In this Primer, we discuss how the brain monitors the water content of the body and then transforms that physical information into the motivation to drink.

Figure 1

Physiologic effects of deviations in plasma osmolality

Figure 2

Intracellular versus extracellular dehydration.

Figure 3. The neural circuit that controls thirst

(A) A set of integrated brain structures called the lamina terminalis monitors the state of the blood and generates appropriate motivational, autonomic, and hormonal responses. The subfornical organ (SFO) and organum vasculosum of the lamina terminalis (OVLT) directly sense circulating factors and, along with the median preoptic nucleus (MnPO), integrate this information and communicate with downstream brain regions. 3V, third ventricle; AC, anterior commissure; F, fornix. (B) The downstream circuit that controls the autonomic and hormonal responses to fluid imbalance relies on projections from the lamina terminalis to the paraventricular nucleus of the hypothalamus (PVH) and the supraoptic nucleus (SON). (C) The downstream circuit that generates thirst is less clear, although many brain regions have been implicated in the central representation of thirst and as relay and effector/output nuclei. These brain regions were identified using Fos mapping studies in rodents and fMRI/PET mapping studies in humans. ACC, anterior cingulate cortex; AP, area postrema; BNST, bed nucleus of the stria terminalis; CeA, central amygdala; INS, insular cortex; NTS, nucleus tractus solitarii; PAG, periaqueductal gray; PBN, parabrachial nucleus; PVT, paraventricular nucleus of the thalamus; RN, raphe nuclei; VLM, ventrolateral motor nucleus.

Figure 4. Hormonal stimuli for thirst

(A) The most potent hormonal stimulus for thirst is angiotensin II (AngII), which is generated when the rate-limiting enzyme renin is secreted by the kidneys in response to hypovolemia or hypotension. Other hormonal stimuli for thirst are secreted by the stomach and pancreas during eating, as well as by the ovaries during pregnancy. Atrial natriuretic peptide, a potent inhibitor of thirst, is secreted by the heart in response to hypertension. (B) The physiological stimuli that induce secretion of thirst-related hormones include changes in plasma volume and pressure, as well as eating and pregnancy. Decreases in blood volume and pressure increase levels of the dipsogenic hormone AngII, whereas increases in blood volume increase levels of the thirst-inhibiting hormone ANP.