The loss of blood volume is detected by cells in the kidneys and triggers thirst for both water and salt via the renin-angiotensin system. Renin-angiotensin system
Hypovolemia leads to activation of the renin angiotensin system (RAS) and is detected by cells in the kidney. When these cells detect decreased blood flow due to the low volume they secrete an enzyme called renin. Renin then enters the blood where it catalyzes a protein called angiotensinogen to angiotensin I. Angiotensin I is then almost immediately converted by an enzyme already present in the blood to the active form of the protein, angiotensin II. Angiotensin II then travels in the blood until it reaches the posterior pituitary gland and the adrenal cortex, where it causes a cascade effect of hormones that cause the kidneys to retain water and sodium, increasing blood pressure. It is also responsible for the initiation of drinking behavior and salt appetite via the subfornical organ. Others
Arterial baroreceptors sense a decreased arterial pressure, and signal to the central nervous system in the area postrema and nucleus tractus solitarii. Cardiopulmonary receptors sense a decreased blood volume, and signal to area postrema and nucleus tractus solitarii. Cellular dehydration and osmoreceptor stimulation
Osmometric thirst occurs when the solute concentration of the interstitial fluid increases. This increase draws water out of the cells, and they shrink in volume.
The solute concentration of the interstitial fluid increases by high intake of sodium in diet or by the drop in volume of extracellular fluids (such as blood plasma and cerebrospinal fluid) due to loss of water through perspiration, respiration, urination and defecation. The increase in interstitial fluid solute concentration causes water to migrate from the cells of the body, through their membranes, to the extracellular compartment, by osmosis, thus causing cellular dehydration.Clusters of cells (osmoreceptors) in the organum vasculosum of the lamina terminalis (OVLT) and subfornical organ (SFO), which lie outside of the blood brain barrier can detect the concentration of blood plasma and the presence of angiotensin II in the blood. They can then activate the median preoptic nucleus which initiates water seeking and ingestive behavior. Destruction of this part of the hypothalamus in humans and other animals results in partial or total loss of desire to drink even with extremely high salt concentration in the extracellular fluids. In addition, there are visceral osmoreceptors which project to the area postrema and nucleus tractus solitarii in the brain. Salt craving
Because sodium is also lost from the plasma in hypovolemia, the bodys need for salt proportionately increases in addition to thirst in such cases. This is also a result of the renin-angiotensin system activation. Elderly
In adults over the age of 50 years, the bodys thirst sensation reduces and continues diminishing with age, putting this population at increased risk of dehydration.