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An osmoreceptor is a sensory receptor primarily found in the hypothalamus of most homeothermic organisms that detects changes in osmotic pressure. Osmoreceptors can be found in several structures, including two of the circumventricular organs – the vascular organ of the lamina terminalis, and the subfornical organ. They contribute to osmoregulation, controlling fluid balance in the body.[1] Osmoreceptors are also found in the kidneys where they also modulate osmolality.

Mechanism of activation in humansEdit

Osmoreceptors are located in the vascular organ of lamina terminalis (VOLT) a circumventricular organ which lacks a blood-brain barrier. They have a defined functionality as neurons that are endowed with the ability to detect extracellular fluid osmolarity. The VOLT is strongly interconnected with the median preoptic nucleus, and together these structures comprise the anteroventral third ventricle region.[2] Osmoreceptors have aquaporin 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/kg, then water will move out of the cell due to osmosis, causing the neuroreceptor to shrink in size. Embedded into the cell membrane are stretch 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 activates voltage-gated sodium channel, which through a complex conformational change, allows more sodium ions to enter the neuron, leading to further depolarisation and an action potential to be generated. This action potential travels along the axon of the neuron, and causes the opening of voltage-dependent calcium channels in the axon terminal. This leads to a Ca2+ influx, due to calcium ions diffusing into the neuron along their electrochemical gradient. The calcium ions binds to the synaptotagmin 1 sub-unit of the SNARE protein attached to the arginine-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 densaEdit

The macula densa region of the kidney's juxtaglomerular apparatus is another modulator of blood osmolality.[5] The macula densa responds to changes in osmotic pressure through changes in the rate of sodium ion (Na+) flow through the nephron. Decreased Na+ flow stimulates tubuloglomerular feedback to autoregulate, a signal (thought to be regulated by adenosine) sent to the nearby juxtaglomerular cells of the afferent arteriole, causing the juxtaglomerular cells to release the protease renin into circulation. Renin cleaves the zymogen angiotensinogen, 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, by angiotensin 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, triggering aldosterone release from the adrenal cortex, direct vasoconstriction, and thirst behaviors originating in the hypothalamus.

See alsoEdit


  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.
  2. ^ Verbalis JG (December 2007). "How does the brain sense osmolality?". Journal of the American Society of Nephrology. 18 (12): 3056–9. doi:10.1681/ASN.2007070825. PMID 18003769.
  3. ^ Binder MD, Hirokawa N, Windhorst U, eds. (2009). "Stretch-inactivated Cation Channel (SIC)". Encyclopedia of Neuroscience. Berlin Heidelberg: Springer. p. 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. Oxford Textbook (Fourth ed.). Oxford, New York: Oxford University Press. ISBN 978-0-19-959254-8.
  5. ^ "The Urinary System".

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