Mechanisms of Fluid Homeostasis Mediated by the Brainstem
I. Robin A. Barraco in Nucleus of the Solitary Tract, 2019
It is well known that the hypothalamus plays an important role on the control of body fluid homeostasis. ADH secretory neurons in the supraoptic nucleus and paraventricular nucleus have been identified as osmoreceptive neurons. The local elevation in osmolality results in the release of ADH by activation of these osmoreceptive secretory neurons so that body water retention is ensured by increasing the water reabsorption in the kidney. This is the most basic reflex mechanism which maintains fluid homeostasis. Numerous reports have been published on the hypothalamic mechanisms that modulate the hypothalamo-hypophyseal antidiuretic system. Recently, evidence has gradually accumulated for peripheral osmoreceptors, located in the visceral organs, as the sensory cues which participate on this control mechanism. As a result, particular emphasis has been laid on a role of peripheral sensory cues that may affect the hypothalamic control mechanism mediating body fluid homeostasis. Thus, the nucleus of the solitary tract (NTS) has attracted considerable interest since primary afferents from these peripheral osmoreceptors project directly to the NTS.
Control of blood vessels: extrinsic control by nerves and hormones
Neil Herring, David J. Paterson in Levick's Introduction to Cardiovascular Physiology, 2018
Osmoreceptors are neurons in the anterolateral hypothalamus that are sensitive to plasma osmolarity. They are located in the organum vasculosum lamina terminalis and subfornicular organ which, appropriately, lack a blood-brain barrier; the capillary endothelium is fenestrated at these sites. The osmoreceptors are excited by a rise in plasma osmolarity above 280-285 mOsm, for example during dehydration. Cholinergic axons extend from the osmoreceptors to synapse with the nearby magnocellular neurons, stimulating them to secrete vasopressin. Since a 2% rise in plasma osmolarity has the same stimulatory effect as a 10% fall in blood volume, vasopressin secretion is more sensitive to plasma osmolarity than blood volume. The osmoreceptors also project to parvocellular (small) neurons in the paraventricular nucleus, which influence sympathetic activity; consequently, water deprivation increases peripheral vasoconstrictor sympathetic activity, as well as vasopressin levels.
Tubular Function
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2020
The release of ADH from the posterior pituitary is under the control of baroreceptor and osmoreceptor reflexes that act via the hypothalamus. Hypothalamic osmoreceptors sense changes in plasma osmotic pressure. A rise in osmotic pressure increases ADH secretion, and a fall in osmotic pressure reduces ADH secretion. The set point of the system is defined as the plasma osmolality at which ADH secretion begins to increase and the slope of this relationship is quite steep, reflecting the sensitivity of the system, and below this, virtually no ADH is released. The set point varies from 280 to 295 mOsm/kg H2O. A fall in plasma volume is detected by arterial, venous and, particularly, cardiac atrial baroreceptors, which reduce their afferent firing rate to the hypothalamus, in turn increasing ADH release from the posterior pituitary. The sensitivity of the baroreceptor mechanism is less than that of osmoreceptors. A 5%–10% decrease in blood volume is required before ADH secretion is stimulated. Changes in blood volume also influence the secretion of ADH in response to changes in plasma osmolality. When a decrease in blood volume occurs, the set point shifts to lower plasma osmolality values and the slope is steeper. This allows the kidney to conserve water, even though the water retention will reduce the osmolality of body fluids. The opposite response occurs with an increase in blood volume and the set point shifts to higher osmolality values and the slope is decreased. The same osmoreceptors and baroreceptors control the sensation of thirst via hypothalamic centres close to those producing ADH.
Activation of tumor cell integrin αvβ3 by radiation and reversal of activation by chemically modified tetraiodothyroacetic acid (tetrac)
Published in Endocrine Research, 2018
John T. Leith, Aleck Hercbergs, Susan Kenney, Shaker A. Mousa, Paul J. Davis
The surprising finding in the current studies is that integrin αvβ3 undergoes a substantial physical change (“activation”) acutely in response to radiation exposure. This change has not previously been described as a feature of cell response to radiation exposure. While such a change is likely to generate intracellular signals via stress-activated protein kinases and other factors cited above, the change may also radically change the complex cell–cell and cell–ECM protein interactions of the integrin. Such changes could involve αvβ3-dependent alterations in cell permeability,24 resulting in cellular osmolar stress that inhibits DNA replication25 and contributes to radioresistance. Integrins are known to be osmoreceptors.26 We also speculate that important radiation-induced changes in abundance and function of cell surface αvβ3 might alter the physical state of tumor cell microenvironment sufficiently to reduce oxygen diffusion and metabolic substrate availability to cells. This would also serve to inhibit cell division and radiosensitivity.
Mechanisms involved in the cardiovascular effects caused by acute osmotic stimulation in conscious rats
Published in Stress, 2020
Eduardo Albino Trindade Fortaleza, Cristiane Busnardo, Aline Fassini, Ivaldo Jesus Almeida Belém-Filho, Gislaine Almeida-Pereira, José Antunes-Rodrigues, Fernando Morgan Aguiar Corrêa
Osmoreceptors are found in forebrain areas, such as the subfornical organ and organum vasculosum of the lamina terminalis (Bourque, 2008; Broadwell & Brightman, 1976; McKinley et al., 1983). Additionally, there are peripheral osmoreceptors in the liver, mouth, splanchnic circulation, and hepatoportal region (Bisset & Chowdrey, 1988; Bourque et al., 1994; Hosomi & Morita, 1996). When stimulated, they activate the hypothalamic supraoptic nucleus (SON) and the paraventricular nucleus (PVN) to regulate vasopressin (AVP) and oxytocin (OT) secretion, and the central sympathetic neurocircuitry (Hussy, Deleuze, Desarmenien, & Moos, 2000; Larsen & Mikkelsen, 1995; Onaka & Yagi, 2001; Weiss & Hatton, 1990), integrating cardiovascular control and body fluid balance (Haberich, 1968; Herbert, Moga, & Saper, 1990; Kobashi & Adachi, 1985; Ricardo & Koh, 1978; Saper, Reis, & Joh, 1983; Sawchenko & Swanson, 1982; Stocker, Osborn, & Carmichael, 2008; Toney, Chen, Cato, & Stocker, 2003; Torvik, 1956; van der Kooy & Koda, 1983).
Psychogenic polydipsia associated with sertraline treatment: a case report
Published in Psychiatry and Clinical Psychopharmacology, 2019
Esra Okyar, Leyla Bozatlı, Işık Görker, Serap Okyar
The regulation of the hypothalamic thirst center is thought to be impaired in the pathogenesis [8]. If the solute concentration in the extracellular fluid increases, the osmoreceptors in the hypothalamus generate an output signal to increase the release of ADH from the posterior pituitary. If the solute concentration in the extracellular fluid decreases, there is a decrease in the release of ADH [14]. It is thought that patients with PP have inappropriate ADH release or inadequate response of kidneys to ADH. While ADH levels are high in PP, the osmotic threshold for ADH release is reduced [8]. Hippocampal dysregulation of fluid consumption behavior is another cause of PP [15].
Related Knowledge Centers
- Circumventricular Organs
- Osmotic Pressure
- Sensory Neuron
- Osmoregulation
- Kidney
- Hypothalamus
- Homeothermy
- Vascular Organ of Lamina Terminalis
- Subfornical Organ
- Fluid Balance