Refers to the craving for fluids, resulting in the basic instinct to drink.
Thirst is an essential mechanism involved in fluid balance, and arises from a lack of fluids or an increase in the concentration of certain osmolites, such as sodium.
When body water volume falls below a certain threshold or the osmolite concentration becomes too high, the brain detects changes in blood constituents and signals thirst.
Thirst starts with the excitation of osmoregulatory cells in the brain called the lamina terminalis.
The lamina terminalis is located in the anterior wall of the third ventricle, and contains three nuclei: the subformical organ, the organ vascululosum, of the lamina terminalis, the median preoptic nucleus.
These nuclei lack a blood brain, barrier and critical for gauging the extent of salinity or osmosensing.
Excitatory neurons in the these areas are crucial for eliciting thirst.
Stimulation of these neurons elicit drinking behavior.
Continuous dehydration is most often associated with renal and neurological disorders.
Excessive thirst, called polydipsia, along with excessive urination, known as polyuria, may be an indication of diabetes mellitus or diabetes insipidus.
Extracellular thirst is generated by decreased volume and intracellular thirst is generated by increased osmolite concentration.
The body’s goal is to keep the interstitial fluid, at the same concentration as the intracellular fluid, isotonic.
Isotonic concentration occurs when the same level of solutes are present on either side of the cell membrane so that the net water movement is zero.
Interstitial fluid with a higher concentration of solutes than the intracellular fluid, water will be pulled out of the cell.
With hypertonic interstial fluid,and if enough water leaves the cell it will not be able to perform essential chemical functions.
If the interstitial fluid becomes less concentrated the cell will fill with water.
This hypotonic situation can be dangerous because it can cause the cell to swell and rupture.
Receptors responsible for thirst detects the concentration of interstitial fluid, and another set of receptors detects blood volume.
Thirst can caused by loss of blood volume, known as hypovolemia, without depleting the intracellular fluid.
Neurons in the lamina terminalis circumstanceventricular organs are unprotected by the blood brain barrier and are primarily responsible for the molecular basis of thirst.
These excitatory neurons drive fluid consumption as corrective behavior, and do so rapidly.
In contrast extracellular volume depletion, or salt loss, stimulate separate sets of neurons, some of which respond to angiotensin II and aldosterone.
Sensory pathways in the brain may explain the preference for electrolyte containing sports drinks after intense exercise.
Pathways in the oral pharynx and gastrointestinal tract monitor water and salt content of recently ingested food and rapidly communicate to the central nervous system thirst centers, creating a high gain, feeding system.
Plasma sodium concentration is tightly controlled by thirst and arginine vasopressin, but the plasma or cerebrospinal fluid sodium concentration has also been postulated to play a role in neurogenic hypertension.
Hypovolemia can be caused by blood loss, vomiting, and diarrhea.
If the total blood volume falls too low the heart cannot circulate blood effectively and the eventual result is hypovolemic shock.
The loss of blood volume is detected by cells in the kidneys..
The loss of volume triggers thirst for both water and salt via the renin-angiotensin system.
Hypovolemia activates the renin angiotensin system (RAS) and is detected by cells in the kidney.
Kidney cells detecting hypovolemia
secrete renin.
Renin is an enzyme that enters the blood where it catalyzes a protein called angiotensinogen to angiotensin I.
Angiotensin I is then almost immediately converted to the active form of the protein, angiotensin II.
Angiotensin II then travels via the blood stream 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.
Angiotensin II also responsible for the initiation of drinking behavior and salt appetite
When arterial and cardiopulmonary baroreceptors sense a decreased arterial pressure, they signal to the central nervous system in the area postrema and nucleus tractus solitarii.
When solute concentration of the interstitial fluid increases osmotic thirst occurs.
Osmotic thirst draws water out of the cells, and they shrink in volume.
The solute concentration of the interstitial fluid is increased by high intake of sodium in diet or by the drop in volume of extracellular fluids due to loss of water through perspiration, respiration, urination and defecation.
Interstitial fluid solute concentration increase causes water to migrate from the cells of the body, through their membranes, to the extracellular compartment, by osmosis, thus causing cellular dehydration.
Osmoreceptor cells in the organum vasculosum of the lamina terminalis (OVLT) and subfornical organ (SFO), which are outside of the blood brain barrier, can recognize the concentration of blood plasma and the presence of angiotensin II in the blood.
Osmoreceptor cells can activate the median preoptic nucleus which initiates water seeking behavior.
Osmoreceptor cell damage in the
hypothalamus results in partial or total loss of desire to drink even with extremely high salt concentration.
Visceral osmoreceptors also exist in the area postrema and nucleus tractus solitarii in the brain.
When sodium is lost from the plasma in hypovolemia, the body’s need for salt proportionately increases in addition to thirst in such cases, and the renin-angiotensin system activates.
After the age of 50 years, the body’s thirst sensation reduces and continues diminish with age.
The older population is at increased risk of dehydration.
The elderly have lower total water intakes than younger adults, and that women are particularly at risk of too low an intake.
Recommended intake volumes in adults (2.0 L/day for females and 2.5 L/day for males).
Water requirement in the elderly group is increased due to a reduction in renal concentrating capacity.
Quenching thirst mechanisms to stop drinking, occurs via two neural phases:
a preabsorption phase which signals quenched thirst many minutes before fluid is absorbed from the stomach and distributed to the body
a postabsorptive phase which is regulated by brain sensing to terminate fluid ingestion.
In the preabsorptive phase sensory input in the mouth, pharynx, esophagus, and upper gastrointestinal tract anticipates the amount of fluid needed, they then provide rapid signals to the brain to terminate drinking when the assessed amount has been consumed.
In the postabsorptive phase blood monitoring for osmolality, fluid volume, and sodium balance, are collectively sensed in brain circumventricular organs linked via neural networks to terminate thirst when fluid balance is established.
Humans may need hours to restore fluid balance.
The areas of the brain that contribute to the sense of thirst are mainly located in the midbrain and the hindbrain, specifically, the hypothalamus.
The area postrema and nucleus tractus solitarii manifest thirst signals to the subfornical organ and to the lateral parabrachial nuclei, and relies on the neurotransmitter serotonin.
The median preoptic nucleus and the subfornical organ of the brain receive signals of decreased volume
and increased osmolite concentration.
Signals are received in cortex areas of the forebrain where thirst arises.