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Osmoreceptor

From Wikipedia, the free encyclopedia
Sensory neuron that detects osmotic pressure changes in warm-blooded organisms
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Anosmoreceptor is asensory receptor primarily found in thehypothalamus of mosthomeothermic organisms that detects changes inosmotic pressure. Osmoreceptors can be found in several structures, including two of thecircumventricular organs – thevascular organ of the lamina terminalis, and thesubfornical organ. They contribute toosmoregulation, controllingfluid balance in the body.[1] Osmoreceptors are also found in thekidneys where they also modulateosmolality.

Mechanism of activation in humans

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Osmoreceptors are located in two of thecircumventricular organs — thevascular organ of lamina terminalis (VOLT) and thesubfornical organ. These two circumventricular organs are located along the anteroventral region of the third ventricle, called the AV3V region.[2] Between these two organs is themedian preoptic nucleus, which has multiple nerve connections with the two organs, as well as with thesupraoptic nuclei and blood pressure control centers in themedulla oblongata.[2]

The osmoreceptors have a defined functionality as neurons that are endowed with the ability to detect extracellular fluidosmolarity. Osmoreceptors haveaquaporin 4 proteins spanning through their plasma membranes in which water can diffuse, from an area of high to low water concentration. If plasma osmolarity rises above 290 mOsmol/L, then water will move out of the cell due to osmosis, causing the neuroreceptor to shrink in size. Embedded into the cell membrane arestretch inactivated cation channels (SICs), which when the cell shrinks in size, open and allow positively charged ions, such as Na+ and K+ ions to enter the cell.[3] This causes initial depolarisation of the osmoreceptor and activatesvoltage-gated sodium channel, which through a complex conformational change, allows more sodium ions to enter the neuron, leading to further depolarisation and anaction potential to be generated. This action potential travels along the axon of the neuron, and causes the opening ofvoltage-dependent calcium channels in the axon terminal. This leads to a Ca2+ influx, due to calcium ions diffusing into the neuron along theirelectrochemical gradient. The calcium ions binds to thesynaptotagmin 1 sub-unit of theSNARE protein attached to thearginine-vasopressin (AVP) containing vesicle membrane. This causes the fusion of the vesicle with the neuronal post synaptic membrane. Subsequent release of AVP into the posterior pituitary gland occurs, whereby vasopressin is secreted into the blood stream of the nearby capillaries.[4]

Macula densa

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Themacula densa region of the kidney'sjuxtaglomerular apparatus is another modulator of bloodosmolality.[5] The macula densa responds to changes in osmotic pressure through changes in the rate ofsodium ion (Na+) flow through thenephron. Decreased Na+ flow stimulatestubuloglomerular feedback to autoregulate, a signal (thought to be regulated byadenosine) sent to the nearbyjuxtaglomerular cells of theafferent arteriole, causing the juxtaglomerular cells to release theproteaserenin into circulation. Renin cleaves thezymogenangiotensinogen, always present in plasma as a result of constitutive production in the liver, into a second inactive form,angiotensin I, which is then converted to its active form,angiotensin II, byangiotensin converting enzyme (ACE), which is widely distributed in the small vessels of the body, but particularly concentrated in the pulmonary capillaries of the lungs.Angiotensin II exerts system wide effects, triggeringaldosterone release from theadrenal cortex, directvasoconstriction, andthirst behaviors originating in thehypothalamus. This is commonly known as therenin-angiotensin-aldosterone system.

See also

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References

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  1. ^Bourque CW (July 2008). "Central mechanisms of osmosensation and systemic osmoregulation".Nature Reviews. Neuroscience.9 (7):519–31.doi:10.1038/nrn2400.PMID 18509340.S2CID 205504313.
  2. ^abHall, John E. (2021).Guyton and Hall textbook of medical physiology. Michael E. Hall (14 ed.). Philadelphia, PA. p. 376.ISBN 978-0-323-59712-8.OCLC 1129099861.{{cite book}}: CS1 maint: location missing publisher (link)
  3. ^Binder MD, Hirokawa N, Windhorst U, eds. (2009). "Stretch-inactivated Cation Channel (SIC)".Encyclopedia of Neuroscience. Berlin Heidelberg: Springer. pp. 3865.doi:10.1007/978-3-540-29678-2_5688.ISBN 978-3-540-23735-8.
  4. ^Turner NN, Lameire N, Goldsmith DJ, Winearls CG, Himmelfarb J, Remuzzi G, Bennet WG, Broe ME, Chapman JR, Covic A, Jha V, Sheerin N, Unwin R, Woolf A, eds. (2015-10-29).Oxford Textbook of Clinical Nephrology (Fourth ed.). Oxford, New York: Oxford University Press.ISBN 978-0-19-959254-8.
  5. ^"The Urinary System".www2.highlands.edu. Archived fromthe original on 2018-04-15. Retrieved2017-09-16.

External links

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