Osmometric Thirst

Published: 2021-09-13 06:15:08
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Thirst is the craving for liquids, resulting in the basic instinct of humans or animals to drink. It is an essential mechanism involved in fluid balance. It arises from a lack of fluids and/or an increase in the concentration of certain osmolites such as salt. If the water volume of the body falls below a certain threshold, or the osmolite concentration becomes too high, the brain signals thirst.
Continuous dehydration can cause a myriad of problems, but is most often associated with neurological problems such as seizures, and renal problems. Excessive thirst, known as polydipsia, along with excessive urination, known as polyuria, may be an indication ofdiabetes. Thirst produced by an increase in the osmotic pressure of the interstitial fluid relative to the intracellular fluid thus producing cellular dehydration fluid, Intracellular fluid, fluid contained within cells.
Osmometric thirst occurs when the osmotic balance between the amount of water in the cells & the water outside the cells becomes disturbed means when the concentration of salts in the interstitial fluid is greater than that inside the cells, resulting in the movement of intracellular water outside of the cell by osmosis. This is what happens when we eat salty pretzels. The Na is absorbed into the blood plasma, which disrupts the osmotic balance between the blood plasma & the interstitial fluid.
This draws water out of the interstitial fluid and into the plasma, now upsetting the balance between the cells and the interstitial fluid. The result is water leaving the cells to restore the balance. The disruption in the interstitial solution is recognized by neurons called osmoreceptors. These osmoreceptors are located in the region of the anterior hypothalamus. These osmoreceptors send a signal that causes us to drink more water, in order to restore the osmotic balance between the cells and surrounding fluid. In the case of pretzel eating, if we do not drink more water, eventually the excess Na is simply excreted by the kidneys.
The body must have water to excrete in order to rid itself of nitrogenous wastes, so the reduction in water excretion causes fluid-seeking behavior. OSMOMETRIC THIRST is stimulated by cellular dehydration. It occurs when the tonicity of the interstitial fluid increases, which draws water out of the cells (think of water seeking to be balanced), cells then shrink in volume. The word “osmosis” means movement of water, through semi permeable membrane, from low solute concentration to high solute concentration. There are receptors and other systems in the body that detect a decreased volume or an increased osmolite concentration.
They signal to the central nervous system, where central processing succeeds. There are some RECEPTORS FOR OSMOMETRIC THIRST (already in the central nervous system more specifically in hypothalamus notably in two circumventrivular organs that lack an effective brain-barrier the organumvasculosum of the lamina terminalis (OVLT) and the subfornical organ (SFO). However, although located in the same parts of the brain, these osmoreceptors that evoke thirst are distinct from the neighboring osmoreceptors in the OVLT and SFO that evoke arginine vasopressin release to decrease fluid output.
In addition, there are visceral osmoreceptors. These project to the area postrema and nucleus tractussolitarius in the brain), the neurons that respond to changes in the solute concentration of the interstitial fluid – start firing when water is drawn out of them due to hyper tonicity; most likely located in the anteroventral tip of the third ventricle (AV3V); if activated, they send signals to neurons that control rate of vasopressin secretion So, the question will be raised such as do we want more or less vasopressin?
We want more vasopressin; remember high levels of vasopressin cause kidneys to retain water, sweating causes loss of water through skin, which increases tonicity of interstitial fluid, which then draws water out of the capillaries and cells.
We can lose water only from the cells, but not intravascular, by eating a salty meal in which salt is absorbed from the digestive tract into the blood, this makes the blood hypertonic (high concentration of salt), this draws water into the cell from the interstitial fluid, the loss of water from the interstitial fluid makes it hypertonic, now water is drawn out of the cells, as blood plasma increases in volume, kidneys excrete more water and sodium, eventually, excess sodium is excreted, along with the water that was taken from the interstitial fluid and intercellular fluid, this results in an overall loss of water from the cells, however, blood plasma volume never decreased.
The damage to AV3V area can cause diabetes and lack of thirst (excessive urination, so must force self to drink) subfornical organ (SFO) – circumventricular organ whose AII receptors are the site where angiotensin acts to produce thirst; it has few neural inputs, as its job is to sense the presence of a hormone in the blood; it has many outputs to various parts of the brain:  endocrine – SFO axons project to neurons in the supraoptic and paraventricular nuclei that are responsible for production and secretion of the posterior pituitary hormone vasopressin  Autonomic – axons project to cells of the paraventricular nucleus and other parts of the hypothalamus, which the send axons to brain stem nuclei which control the sympathetic and parasympathetic nervous system; this system controls angiontensin’s effect on blood pressure. behavioral – axons sent to median preoptic nucleus, an area which controls drinking and secretion of vasopressin median preoptic nucleus – receives information from: 1. OVLT regarding osmoreceptors 2. SFO regarding angiotensin.
Baroreceptors via the nucleus of the solitary tract Lateral Hypothalamus and Zona Incerta esions of the hypothalamus disrupt osmometric and volumetric thirst, but not meal-associated drinking lesions of the zona incerta disrupt hormonal stimulus for volumetric thirst, but not the neural ones that originate in the atrial baroreceptors zona incerta sends axons to brain structures involved in movement – influences drinking behavior Central processing The area postrema and nucleus tractussolitarius signal, by 5-HT, to lateral parabrachial nucleus, which in turn signal to median preoptic nucleus. In addition, the area postrema and nucleus tractussolitarius also signal directly to subfornical organ. Thus, the median preoptic nucleus and subfornical organ receive signals of both decreased volume and increased osmolite concentration. They signal to higher integrative centers, where ultimately the conscious craving arises. However, the true neuroscience of this conscious craving is not fully clear.
In addition to thirst, the organumvasculosum of the lamina terminalis and the subfornical organ contribute to fluid balance by vasopressin release. Studies done…. Some research and study presents a theoretical model for osmotic (cellular dehydration) thirst, and evaluates several of the implications of the model. Ss were 11 male Sprague-Dawley rats. The model for osmotic thirst asserts that when a load consisting of n millimols of effective osmotic solute dissolved in v ml. of water is introduced into the extracellular compartment, the S will drink a volume of water, D (in ml. ), which is proportional to the volume of water, Diso (in ml. ), required to dilute the hypertonic load to isotonicity (ALPHA).
Thus, D = k (Diso) = k-n/a-v=, where k is the constant of proportionately representing the contribution of the kidney to osmotic regulation. The experimental data show that under conditions of osmotic thirst this model accurately predicts the rat’s drinking behavior. Osmoregulatory thirst associated with deficits of intracellular fluid volume. Small increases of 1–2% in the effective osmotic pressure of plasma result in stimulation of thirst in mammals. It has been shown in both human subjects and other mammals that when the plasma osmolality (usually in the range of 280–295 mosmol/kgH2O) is increased experimentally as a result of increasing the concentration of solutes such as NaCl or sucrose that do not readily pass across cell membranes, thirst is stimulated.
By contrast, increasing plasma osmolality by systemic infusion of concentrated solutes such as urea or D-glucose that more readily cross nerve cell membranes is relatively ineffective at stimulating thirst (8,12, 18). In the former case, a transmembrane osmotic gradient is established and cellular dehydration results from movement of water out of cells by osmosis. Cellular dehydration does not occur with the permeating solutes in the latter case, and it is considered that specific sensor cells in the brain, termed osmoreceptors (initially in relation to vasopressin secretion), respond to cellular dehydration to initiate neural mechanisms that result in the generation of thirst (8, 18).
Although there is evidence that some osmoreceptors may be situated in the liver, much evidence has accrued that localizes an important population of osmoreceptive neurons to the preoptic/hypothalamic region of the brain. The hypothalamus was implicated in the generation of thirst in the early 1950s when Bengt Andersson was able to stimulate water drinking in goats by electrical or chemical stimulation of the hypothalamus. Although he observed that drinking was induced by injection of hypertonic saline into the hypothalamus in a region between the columns of the fornix and the mamillothalamic tract, the solutions injected were grossly hypertonic, making it difficult to come to a firm conclusion that physiologically relevant osmoreceptors for thirst existed in this region.
Andersson and colleagues later found evidence that more rostral tissue in the anterior wall of the third ventricle was more likely to be the site of sensors mediating osmotic thirst and proposed a role for the ambient Na+ concentration in this region of the brain in the initiation of thirst. Neural mechanisms sub serving osmotically stimulated thirst… More than 25 years ago, clues emerged as to the crucial role of a region in the anterior wall of the third ventricle in thirst mechanisms when it was shown that ablation of tissue in the anteroventral third ventricle wall (AV3V region) of goats and rats caused either temporary or permanent adipsia (1, 10). In those animals with lesions that did recover spontaneous water drinking, loss of dipsogenic responsiveness to osmotic and ANG stimuli was evident.
Another clue to the location of cerebral osmoreceptors sub serving thirst came from studies in sheep suggesting that the cerebral osmoreceptors sub serving thirst and vasopressin secretion were, at least in part, located in brain regions lacking a blood-brain barrier. In subsequent years, evidence (reviewed in Ref. 14) from the study of lesions, electrophysiological recordings, and the expression of the immediate early gene c-fos in rats have confirmed that neurons in both the organum vasculosum of the lamina terminalis (OVLT) and the subfornical organ (SFO) are most likely the sites of very sensitive osmoreceptors (Fig. 1? ). The SFO and OVLT are two circumventricular organs that lack a blood-brain barrier and that are situated in the anterior wall of the third ventricle (the lamina terminalis). In particular, the dorsal part of the OVLT and the periphery of the SFO are osmosensitive in the rat.
However, the median preoptic nucleus (MnPO), which is situated in the lamina terminalis longitudinally between the two circumventricular organs and is an integral part of the AV3V region, is also strongly activated by osmotic stimuli. Lesion studies in rats have shown that the MnPO may play a crucial role in the generation of thirst in response to both osmotic and hormonal signals being relayed to this nucleus by neural inputs from the SFO and possibly the OVLT (10). Another aspect of osmoregulatory drinking is that it may be blocked pharmacologically by intracerebroventricularly injected ANG antagonists, suggesting that a central angiotensinergic pathway is involved in most mammals. The MnPO, which is rich in ANG type 1 receptors but is not amenable to circulating ANG II, is a likely site of this angiotensinergic synapse.
The MnPO receives afferent neural input from neurons in both the SFO and the OVLT and may integrate neural signals coming from osmoreceptive neurons in these circumventricular organs with visceral sensory inflow from the hindbrain However, combined ablation of both the SFO and OVLT leaving a considerable part of the MnPO intact reduces but does not totally abolish osmotically induced drinking. This suggests that neurons within the MnPO may be osmoreceptive also or that they receive osmotically related input from other parts of the brain [e. g. , the area postrema (AP)] or body (e. g. , hepatic portal system). It is clear that the lamina terminalis is a region of the brain where stimuli from the circulation, such as plasma hypertonicity or hormones (e. g. , ANG II, relaxin), exert their dipsogenic action.
In regard to the subsequent efferent neural pathways that may project from the lamina terminalis to other brain regions (including the cerebral cortex) to generate thirst, little is known at present. The lateral hypothalamic area, the hypothalamic paraventricular nucleus, and the periaqueductal gray are all regions that receive a strong neural input from the lamina terminalis and have been proposed as regions that may participate in the generation of thirst. However, evidence in support of such proposals is scarce. Recent studies using positron emission tomography in human volunteers identified several brain regions that became activated during an intravenous infusion of hypertonic saline that produced a strong thirst sensation in these subjects.
In particular, the anterior and posterior parts of the cingulate cortex were activated, and on satiation of the thirst, these areas rapidly declined in activity. This cingulate region has been implicated in other goal-directed behaviors and probably plays a yet-to-be-specified role in the generation of human thirst. Angiotensin and thirst Classic studies by Fitzsimons and associates (see Ref. 8 for review) were the first to clearly demonstrate that renin and its effector peptide, ANG II, were highly effective as dipsogenic stimuli in the rat. Systemically administered renin or ANG II generates water intake in sated rats.
As is true for osmotically stimulated drinking, ANG-induced thirst requires the structures of the lamina terminalis (i. e. SFO, MnPO, and OVLT) for sensing circulating peptides (particularly the SFO) and for initial central nervous system processing and integration of this peripherally derived information (10). The dipsogenic action of ANG is even more impressive when it is injected directly into the brain, and this has been demonstrated in several mammals (rat, goat, dog, sheep) and also in birds (duck, pigeon). This route of administration is believed to mimic the action of this peptide at one or more periventricular brain sites. The presence of a brain renin-angiotensin system with all the components of the metabolic cascade as well as receptors being synthesized de novo in the brain has been demonstrated.
It has been hypothesized that circulating ANG II acts on forebrain circumventricular organs (SFO, OVLT) in the mode of a hormone and that, either directly or indirectly, it activates angiotensinergic pathways projecting to central integrative sites when the peptide acts as a neurotransmitter (11). The systemic (renal/circulating) and the brain renin-angiotensin systems, although distinct, are functionally coupled with one another and play complementary roles in the maintenance of body fluid homeostasis. Inhibition and facilitation of thirst through hindbrain actions In addition to humoral factors acting through forebrain targets and networks to facilitate drinking, there is evidence of both stimulatory and inhibitory signals acting on or through the hindbrain.
When the hypertension induced by intravenous ANG II in rats is reduced or normalized by coadministration of a systemically acting hypotensive drug, drinking responses to infusions of ANG II are enhanced (7). In rats with actions of the systemic renin-angiotensin system blocked, reducing blood pressure to below normal resting levels enhances the drinking response to intracerebroventricular ANG II infusions (11). Inhibition of thirst arises not only from arterial baroreceptors but also from volume receptors on the low-pressure side of the circulation. Distention of the region of the junction of the right atrium and vena cava or of the pulmonary vein at the entry to the left atrium by inflating balloons inhibits experimentally induced drinking.
In contrast, when, in ogs, both low-pressure cardiopulmonary and high-pressure arterial baroreceptors are unloaded by reducing venous return to the heart, drinking is stimulated (9, 17). Under such conditions, Quillen and colleagues (15) found that denervation of either the cardiopulmonary or sinoaortic baroreceptors significantly attenuated thirst in the dog and that denervation of both sets of receptors completely abolished drinking even though circulating levels of ANG were high. Afferent input from the cardiopulmonary and arterial baroreceptors is carried to the brain by the IXth and Xth cranial nerves, with most of these nerves terminating in the nucleus of the solitary tract (NTS).
Lesions centered on the AP, but also encroaching on the medial portions of the medial NTS (i. e. , an AP/mNTS lesion), as well as bilateral lesions centering on the medial subnucleus of the NTS proper, produce rats that overrespond to thirst-inducing treatments associated with hypovolemia (5). These effects are likely to be due to removal of inhibitory baroreceptor-derived input. However, it is possible that the AP also plays a role in the inhibitory control of thirst derived from systemic blood volume expansion or acute hypertension. As demonstrated by Antunes-Rodrigues and colleagues (2), a peptide made and released from the cardiac atria, ANP, inhibits drinking.
Release of ANP in response to hypervolemia and hypertension may inhibit drinking. Its action is discussed below. Interestingly, the AP/NTS region contains cells with axons that project to the lateral parabrachial nucleus (LPBN). Electrolytic, anesthetic, and neurotoxic lesions of the LPBN produce overdrinking to mediators of extracellular dehydration in the rat (11). This is similar to the effects of AP/mNTS lesions. A significant portion of the cells that project from the AP/mNTS to the LPBN contain serotonin (5-HT), and bilateral injections of the nonselective 5-HT receptor antagonist methysergide enhance drinking as well as NaCl solution intake in response to several dipsogenic stimuli in rats (see Ref. 11 for review).
The model that has been proposed is that there is a hindbrain inhibitory circuit involving the AP, NTS, and LPBN that receives and processes neural and humoral input derived from activation of cardiopulmonary and arterial baroreceptors. Ascending pathways from this inhibitory complex project to many forebrain structures, such as the structures along the lamina terminalis, the central nucleus of the amygdala, and various hypothalamic nuclei that have been implicated in thirst. In turn, many of these forebrain structures have reciprocal connections with the LPBN and NTS. It is within this visceral neural network where the input from both excitatory and inhibitory humoral and visceral afferent nerves is likely to be processed to give rise to drinking behaviors or the perception of thirst.

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