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Vasopressin

From Wikipedia, the free encyclopedia

This article is about the natural peptide in humans. For the medication, seeVasopressin (medication).
Not to be confused withvasopressorsgenerally, of which it is but one example.
Vasopressin
Clinical data
Pronunciation/ˌveɪzoʊˈprɛsɪn/
Other namesAntidiuretic hormone (ADH); arginine vasopressin (AVP); argipressin
ATC code
Physiologicaldata
SourcetissuesSupraoptic nucleus;paraventricular nucleus of hypothalamus
Target tissuesSystem-wide
ReceptorsV1A,V1B,V2,OXTR
AgonistsFelypressin,desmopressin
AntagonistsDiuretics
MetabolismPredominantly in theliverandkidneys
Pharmacokineticdata
Protein binding1%
MetabolismPredominantly in theliverandkidneys
Eliminationhalf-life10–20 minutes
ExcretionUrine
Identifiers
  • 1-{[(4R,7S,10S,13S,16S,19R)-19-Amino-7-(2-amino-2-oxoethyl)-10-(3-amino-3-oxopropyl)-13-benzyl-16-(4-hydroxybenzyl)-6,9,12,15,18-pentaoxo-1,2-dithia-5,8,11,14,17-pentaazacycloicosan-4-yl]carbonyl}-L-p rolyl-L-arginylglycinamide
CAS Number
PubChemCID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
CompTox Dashboard(EPA)
Chemical and physical data
FormulaC46H65N15O12S2
Molar mass1084.24g·mol−1
3D model (JSmol)
Density1.6±0.1 g/cm3
  • c1ccc(cc1)C[C@H]2C(=O)N[C@H](C(=O)N[C@H](C(=O)N[C@@H](CSSC[C@@H](C(=O)N[C@H](C(=O)N2)Cc3ccc(cc3)O)N)C(=O)N4CCC[C@H]4C(=O)N[C@@H](CCCN=C(N)N)C(=O)NCC(=O)N)CC(=O)N)CCC(=O)N
  • InChI=1S/C46H65N15O12S2 /c47-27-22-74-75-23-33(45(73)61-17-5-9-34(61)44(72)56-28(8-4-16-53-46(51)52)39(67)54-21-37(50)65)60-43(71)32(20-36(49)64)59-40(68)29(14-15-35(48)63)55-41(69)31(18-24-6-2-1-3-7-24)58-42(70)30(57-38(27)66)19-25-10-12-26(62)13-11-25/h1-3,6-7,10-13,27-34,62H,4-5,8-9,14-23,47H2,(H2,48,63)(H2,49,64)(H2,50,65)(H,54,67)(H,55,69)(H,56,72)(H,57,66)(H,58,70)(H,59,68)(H,60,71)(H4,51,52,53)/t27-,28-,29-,30-,31-,32-,33-,34-/m0/s1checkY
  • Key:KBZOIRJILGZLEJ-LGYYRGKSSA-NcheckY
AVP
Identifiers
AliasesAVP,ADH, ARVP, AVP-NPII, AVRP, VP, AVP gene, AVP (gene), Prepro-AVP-NP II, arginine vasopressin gene, vasopressin gene, prepro-arginine-vasopressin-neurophysin II gene, vasopressin-neurophysin II-copeptin, vasopressin-neurophysin 2-copeptin, prepro-AVP2
External IDsOMIM:192340;MGI:88121;HomoloGene:417;GeneCards:AVP;OMA:AVP - orthologs
Orthologs
SpeciesHumanMouse
Entrez

551

11998

Ensembl

ENSG00000101200

ENSMUSG00000037727

UniProt

P01185

P35455

RefSeq (mRNA)

NM_000490

NM_009732

RefSeq (protein)

NP_000481

NP_033862

Location (UCSC)Chr 20: 3.08 – 3.08 MbChr 2: 130.42 – 130.42 Mb
PubMedsearch[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

Humanvasopressin,also calledantidiuretic hormone(ADH),arginine vasopressin(AVP) orargipressin,[5]is ahormonesynthesized from theAVP geneas apeptideprohormoneinneuronsin thehypothalamus,[6]and is converted to AVP. It then travels down theaxonterminating in theposterior pituitary,and is released fromvesiclesinto the circulation in response to extracellular fluidhypertonicity(hyperosmolality). AVP has two primary functions. First, it increases the amount of solute-free water reabsorbed back into thecirculationfrom the filtrate in thekidney tubulesof thenephrons.Second, AVP constrictsarterioles,which increasesperipheral vascular resistanceand raises arterialblood pressure.[7][8][9]

A third function is possible. Some AVP may be released directly into thebrainfrom the hypothalamus, and may play an important role insocial behavior,sexual motivationandpair bonding,and maternal responses to stress.[10]

Vasopressin induces differentiation of stem cells intocardiomyocytesand promotes heart muscle homeostasis.[11]

It has a very short half-life, between 16 and 24 minutes.[9]

Physiology

[edit]
Further information:Renal physiology

Function

[edit]

Vasopressin regulates thetonicityof body fluids. It is released from the posterior pituitary in response tohypertonicityand causes the kidneys to reabsorb solute-free water and return it to the circulation from the tubules of the nephron, thus returning the tonicity of the body fluids toward normal. An incidental consequence of this renal reabsorption of water is concentratedurineand reduced urine volume. AVP released in high concentrations may also raise blood pressure by inducing moderatevasoconstriction.[12]

AVP also may have a variety of neurological effects on the brain. It may influence pair-bonding involes.The high-density distributions of vasopressin receptor AVPr1a inprairie voleventral forebrain regions have been shown to facilitate and coordinate reward circuits during partner preference formation, critical for pair bond formation.[13]

A very similar substance,lysine vasopressin(LVP) orlypressin,has the same function inpigsand its synthetic version was used in human AVP deficiency, although it has been largely replaced bydesmopressin.[14]

Kidney

[edit]

Vasopressin has three main effects which are:

  1. Increasing the water permeability of distal convoluted tubule (DCT) and cortical collecting tubules (CCT), as well as outer and inner medullary collecting duct (OMCD & IMCD) in the kidney, thus allowing water reabsorption and excretion of more concentrated urine, i.e.,antidiuresis.This occurs through increased transcription and insertion of water channels (Aquaporin-2) into theapical membraneof collecting tubule and collecting duct epithelial cells.[15]Aquaporins allow water to move down their osmotic gradient and out of the nephron, increasing the amount of water re-absorbed from the filtrate (forming urine) back into the bloodstream. This effect is mediated byV2 receptors.Vasopressin also increases the concentration of calcium in the collecting duct cells, by episodic release from intracellular stores. Vasopressin, acting throughcAMP,also increases transcription of the aquaporin-2 gene, thus increasing the total number of aquaporin-2 molecules in collecting duct cells.[16]
  2. Increasing permeability of the inner medullary portion of the collecting duct toureaby regulating the cell surface expression ofurea transporters,[17]which facilitates its reabsorption into themedullary interstitiumas it travels down the concentration gradient created by removing water from theconnecting tubule,cortical collecting duct,andouter medullary collecting duct.
  3. Acute increase ofsodiumabsorption across the ascendingloop of Henle.This adds to thecountercurrent multiplicationwhich aids in proper water reabsorption later in thedistal tubuleandcollecting duct.[18]

The hormonevasopressinalso stimulates the activity ofNKCC2.Vasopressin stimulates sodium chloride reabsorption in the thick ascending limb of the nephron by activating signaling pathways. Vasopressin increases the traffic of NKCC2 to the membrane and phosphorylates someserineandthreoninesites on the cytoplasmic N-terminal of the NKCC2 located in the membrane, increasing its activity. Increased NKCC2 activity aids in water reabsorption in the collecting duct throughaquaporin 2channels by creating a hypo-osmotic filtrate.[19][20]

Central nervous system

[edit]

Vasopressin released within the brain may have several actions:

  • Vasopressin is released into the brain in acircadian rhythmby neurons of thesuprachiasmatic nucleus.[21]
  • Vasopressin released from posterior pituitary is associated with nausea.[22]
  • Recent evidence suggests that vasopressin may have analgesic effects. The analgesia effects of vasopressin were found to be dependent on both stress and sex.[23]

Regulation

[edit]

Gene regulation

[edit]
Further information:AVP gene

Vasopressin is regulated byAVPgeneexpression which is managed by major clock controlled genes. In this circadian circuit known as thetranscription-translation feedback loop(TTFL),Per2protein accumulates and is phosphorylated byCK1E.Per2 subsequently inhibits the transcription factorsClockandBMAL1in order to reduce Per2 protein levels in the cell.[24]At the same time, Per2 also inhibits the transcription factors for theAVPgene in order to regulate its expression, the expression of vasopressin, and otherAVPgene products.[25]

Many factors influence the secretion of vasopressin:

  • Ethanol(alcohol) reduces the calcium-dependent secretion of AVP by blocking voltage-gated calcium channels in neurohypophyseal nerve terminals in rats.[26]
  • AngiotensinII stimulates AVP secretion, in keeping with its general pressor and pro-volumic effects on the body.[27]
  • Atrial natriuretic peptideinhibits AVP secretion, in part by inhibiting Angiotensin II-induced stimulation of AVP secretion.[27]
  • Cortisolinhibits secretion of antidiuretic hormone.[28]

Production and secretion

[edit]

The physiological stimulus for secretion of vasopressin is increased osmolality of the plasma, monitored by the hypothalamus. A decreased arterialblood volume,(such as can occur incirrhosis,nephrosis,andheart failure), stimulates secretion, even in the face of decreased osmolality of the plasma: it supersedes osmolality, but with a milder effect. In other words, vasopressin secretion is also stimulated in the presence of hypoosmolality (hyponatremia) when the arterial blood volume is low by the unloading ofbaroreceptors.[29]

The AVP that is measured in peripheral blood is almost all derived from secretion from theposterior pituitary gland(except in cases of AVP-secreting tumours). Vasopressin is produced bymagnocellular neurosecretory neuronsin theparaventricular nucleus of hypothalamus(PVN) andsupraoptic nucleus(SON). It then travels down the axon through theinfundibulumwithin neurosecretory granules that are found within Herring bodies, localized swellings of the axons and nerve terminals. These carry the peptide directly to the posterior pituitary gland, where it is stored until released into the blood.

There are other sources of AVP, beyond the hypothalamic magnocellular neurons. For example, AVP is also synthesized byparvocellular neurosecretory neuronsof the PVN, transported and released at themedian eminence,from which it travels through thehypophyseal portal systemto the anterior pituitary, where it stimulatescorticotropic cellssynergistically with CRH to produce ACTH (by itself it is a weak secretagogue).[30]

Vasopressin during surgery and anaesthesia

[edit]

Vasopressin concentration is used to measuresurgical stressfor evaluation of surgical techniques. Plasma vasopressin concentration is elevated bynoxious stimuli,[31][32]predominantly during abdominal surgery,[33][34][35]especially at gut manipulation, traction of viscera,[36][37][38]as well as abdominal insufflation with carbon dioxide during laparoscopic surgery.[39][40]

Receptors

[edit]

Types of AVP receptors and their actions:

Type Second messenger system Locations Actions Agonists Antagonists
AVPR1A Phosphatidylinositol/calcium Liver,kidney,peripheral vasculature,brain Vasoconstriction,glycogenbreakdown,[41]plateletaggregation, and release offactor VIIIandvon Willebrand factor;social recognition,[42]circadian tau[43] Felypressin
AVPR1B or AVPR3 Phosphatidylinositol/calcium Pituitary gland,brain Adrenocorticotropic hormonesecretion in response to stress;[44]social interpretation of olfactory cues[45]
AVPR2 Adenylate cyclase/cAMP Basolateral membrane of the cells lining thecollecting ductsof the kidneys (especially the cortical and outer medullary collecting ducts) Insertion ofaquaporin-2(AQP2) channels (water channels). This allows water to be reabsorbed down an osmotic gradient, and so the urine is more concentrated. Release ofvon Willebrand factorand surface expression ofP-selectinthrough exocytosis ofWeibel-Palade bodiesfromendothelial cells[46][47] AVP,desmopressin "-vaptan" diuretics, i.e.tolvaptan

Structure and relation to oxytocin

[edit]
Chemical structure of the arginine vasopressin (argipressin) with anarginineat the 8thamino acidposition. Lysine vasopressin differs only in having alysinein this position.
Chemical structure ofoxytocin.Differs from AVP at only the 3rd and 8th position.

The vasopressins arepeptidesconsisting of nineamino acids(nonapeptides). The amino acid sequence of arginine vasopressin (argipressin) isCys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2,with the cysteine residues forming adisulfide bondand theC-terminus of the sequence converted to aprimary amide.[48]Lysine vasopressin (lypressin) has alysinein place of the arginine as the eighth amino acid, and is found inpigsand some related animals, whereas arginine vasopressin is found in humans.[49]

The structure ofoxytocinis very similar to that of the vasopressins: It is also a nonapeptide with a disulfide bridge and its amino acid sequence differs at only two positions. The two genes are located on the same chromosome separated by a relatively small distance of less than 15,000 bases in most species. Themagnocellular neuronsthat secrete vasopressin are adjacent to magnocellular neurons that secrete oxytocin, and are similar in many respects. The similarity of the two peptides can cause some cross-reactions: oxytocin has a slight antidiuretic function, and high levels of AVP can cause uterine contractions.[50][51]

Comparison of vasopressin and oxytocin neuropeptide families:

VertebrateVasopressin Family
Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2 Argipressin(AVP, ADH) Mostmammals
Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Lys-Gly-NH2 Lypressin(LVP) Pigs,hippos,warthogs,somemarsupials
Cys-Phe-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2 Phenypressin Somemarsupials
Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Arg-Gly-NH2 Vasotocin† Non-mammals
Vertebrate Oxytocin Family
Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-Gly-NH2 Oxytocin(OXT) Most mammals,ratfish
Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Pro-Gly-NH2 Prol-Oxytocin SomeNew World monkeys,northern tree shrews
Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Ile-Gly-NH2 Mesotocin Most marsupials, allbirds,reptiles,amphibians,lungfishes,coelacanths
Cys-Tyr-Ile-Gln-Ser-Cys-Pro-Ile-Gly-NH2 Seritocin Frogs
Cys-Tyr-Ile-Ser-Asn-Cys-Pro-Ile-Gly-NH2 Isotocin Bony fishes
Cys-Tyr-Ile-Ser-Asn-Cys-Pro-Gln-Gly-NH2 Glumitocin skates
Cys-Tyr-Ile-Asn/Gln-Asn-Cys-Pro-Leu/Val-Gly-NH2 Various tocins Sharks
InvertebrateVP/OT Superfamily
Cys-Leu-Ile-Thr-Asn-Cys-Pro-Arg-Gly-NH2 Inotocin Locust
Cys-Phe-Val-Arg-Asn-Cys-Pro-Thr-Gly-NH2 Annetocin Earthworm
Cys-Phe-Ile-Arg-Asn-Cys-Pro-Lys-Gly-NH2 Lys-Connopressin Geography & imperialcone snail,pond snail,sea hare,leech
Cys-Ile-Ile-Arg-Asn-Cys-Pro-Arg-Gly-NH2 Arg-Connopressin Striped cone snail
Cys-Tyr-Phe-Arg-Asn-Cys-Pro-Ile-Gly-NH2 Cephalotocin Octopus
Cys-Phe-Trp-Thr-Ser-Cys-Pro-Ile-Gly-NH2 Octopressin Octopus
†Vasotocin is the evolutionary progenitor of all the vertebrate neurohypophysial hormones.[52]

Medical use

[edit]
Main article:Vasopressin (medication)

Vasopressin is used to manage anti-diuretic hormone deficiency. Vasopressin is used to treatdiabetes insipidusrelated to low levels of antidiuretic hormone. It is available as Pressyn.[53]

Vasopressin has off-label uses and is used in the treatment of vasodilatory shock, gastrointestinal bleeding,ventricular tachycardiaand ventricular fibrillation.

Vasopressin agonists are used therapeutically in various conditions, and its long-acting synthetic analoguedesmopressinis used in conditions featuring low vasopressin secretion, as well as for control of bleeding (in some forms ofvon Willebrand diseaseand in mildhaemophilia A) and in extreme cases of bedwetting by children.Terlipressinand related analogues are used asvasoconstrictorsin certain conditions. Use of vasopressin analogues foresophageal varicescommenced in 1970.[54]

Vasopressin infusions are also used as second line therapy forseptic shockpatients not responding to fluid resuscitation or infusions ofcatecholamines(e.g.,dopamineornorepinephrine) to increase the blood pressure while sparing the use of catecholamines. These argipressins have much shorter elimination half-life (around 20 minutes) comparing to synthetic non-arginine vasopresines with much longer elimination half-life of many hours. Further, argipressins act on V1a, V1b, and V2 receptors which consequently lead to higher eGFR and lower vascular resistance in the lungs. A number of injectable arginine vasopressins are currently in clinical use in the United States and in Europe.

Pharmacokinetics

[edit]

Vasopressin is administered through anintravenous device,intramuscular injectionor asubcutaneous injection.Theduration of actiondepends on the mode of administration and ranges from thirty minutes to two hours. It has ahalf lifeof ten to twenty minutes. It is widely distributed throughout the body and remains in theextracellular fluid.It is degraded by theliverand excreted through thekidneys.[53]Arginin vasopressins for use in septic shock are intended for intravenous use only.

Side effects

[edit]

The most common side effects during treatment with vasopressin aredizziness,angina,chest pain, abdominal cramps,heartburn,nausea,vomiting,trembling,fever,water intoxication,pounding sensation in the head,diarrhoea,sweating, paleness, andflatulence.The most severe adverse reactions aremyocardial infarctionandhypersensitivity.[53]

Contraindications

[edit]

The use of lysine vasopressin is contraindicated in the presence of hypersensitivity to beef or pork proteins, increasedBUNand chronickidney failure.It is recommended that it be cautiously used in instances of perioperativepolyuria,sensitivity to the drug, asthma, seizures, heart failure, a comatose state, migraine headaches, and cardiovascular disease.[53]

Interactions

[edit]

Deficiency

[edit]

Decreased AVP release (neurogenic — i.e. due to alcohol intoxication or tumour) or decreased renal sensitivity to AVP (nephrogenic, i.e. by mutation of V2 receptor or AQP) leads todiabetes insipidus,a condition featuringhypernatremia(increased bloodsodiumconcentration),polyuria(excess urine production), andpolydipsia(thirst).

Excess

[edit]
Main article:Syndrome of inappropriate antidiuretic hormone secretion

Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH)in turn can be caused by a number of problems. Some forms ofcancercan cause SIADH, particularlysmall cell lung carcinomabut also a number of other tumors. A variety of diseases affecting the brain or the lung (infections, bleeding) can be the driver behind SIADH. A number of drugs have been associated with SIADH, such as certain antidepressants (serotonin reuptake inhibitorsandtricyclic antidepressants), the anticonvulsantcarbamazepine,oxytocin(used to induce and stimulate labor), and the chemotherapy drugvincristine.It has also been associated withfluoroquinolones(includingciprofloxacinandmoxifloxacin).[9]Finally, it can occur without a clear explanation.[55]Hyponatremia can be treated pharmaceutically through the use ofvasopressin receptor antagonists.[55]

History

[edit]

Vasopressin was elucidated and synthesized for the first time byVincent du Vigneaud.

Animal studies

[edit]

Evidence for an effect of AVP on monogamy vs polygamy comes from experimental studies in several species, which indicate that the precise distribution of vasopressin and vasopressin receptors in the brain is associated with species-typical patterns of social behavior. In particular, there are consistent differences between monogamous species and polygamous species in the distribution of AVP receptors, and sometimes in the distribution of vasopressin-containing axons, even when closely related species are compared.[56]

Human studies

[edit]

Vasopressin has shownnootropiceffects on pain perception and cognitive function.[57]Vasopressin also plays a role inautism,major depressive disorder,bipolar disorder,andschizophrenia.[58]

See also

[edit]

References

[edit]
  1. ^abcGRCh38: Ensembl release 89: ENSG00000101200–Ensembl,May 2017
  2. ^abcGRCm38: Ensembl release 89: ENSMUSG00000037727–Ensembl,May 2017
  3. ^"Human PubMed Reference:".National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^"Mouse PubMed Reference:".National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^Anderson DA (2012).Dorland's Illustrated Medical Dictionary(32nd ed.). Elsevier.ISBN978-1-4160-6257-8.
  6. ^Sukhov RR, Walker LC, Rance NE, Price DL, Young WS 3rd (1993)."Vasopressin and oxytocin gene expression in the human hypothalamus".Journal of Comparative Neurology.337(2): 295–306.doi:10.1002/cne.903370210.PMC9883978.PMID8277003.S2CID35174328.
  7. ^Marieb E (2014).Anatomy & physiology.Glenview, IL: Pearson Education, Inc.ISBN978-0-321-86158-0.
  8. ^Caldwell HK, Young WS III (2006)."Oxytocin and Vasopressin: Genetics and Behavioral Implications"(PDF).In Lajtha A, Lim R (eds.).Handbook of Neurochemistry and Molecular Neurobiology: Neuroactive Proteins and Peptides(3rd ed.). Berlin: Springer. pp. 573–607.ISBN978-0-387-30348-2.
  9. ^abcBabar SM (October 2013). "SIADH associated with ciprofloxacin".The Annals of Pharmacotherapy.47(10): 1359–63.doi:10.1177/1060028013502457.PMID24259701.S2CID36759747.
  10. ^Insel TR (March 2010)."The challenge of translation in social neuroscience: a review of oxytocin, vasopressin, and affiliative behavior".Neuron.65(6): 768–79.doi:10.1016/j.neuron.2010.03.005.PMC2847497.PMID20346754.
  11. ^Costa A, Rossi E, Scicchitano BM, Coletti D, Moresi V, Adamo S (September 2014)."Neurohypophyseal Hormones: Novel Actors of Striated Muscle Development and Homeostasis".review.European Journal of Translational Myology.24(3): 3790.doi:10.4081/bam.2014.3.217.PMC4756744.PMID26913138.
  12. ^Cuzzo B, Padala SA, Lappin SL (2024)."Physiology, Vasopressin".StatPearls.StatPearls Publishing.PMID30252325.
  13. ^Lim MM, Young LJ (2004). "Vasopressin-dependent neural circuits underlying pair bond formation in the monogamous prairie vole".Neuroscience.125(1): 35–45.doi:10.1016/j.neuroscience.2003.12.008.PMID15051143.S2CID16210017.
  14. ^Chapman IM, Professor of Medicine, Discipline of Medicine, University of Adelaide, Royal Adelaide Hospital."Central Diabetes Insipidus".MSD.Merck & Co. Inc.
  15. ^Boron WR, Boulpaep EL (2016-05-05).Medical Physiology(Third ed.). Philadelphia, PA: Elsevier.ISBN978-1-4557-4377-3.OCLC951680737.
  16. ^Wilson JL, Miranda CA, Knepper MA (2013)."Vasopressin and the Regulation of Aquaporin-2".Clinical and Experimental Nephrology.17(6): 10.1007/s10157-013–0789-5.doi:10.1007/s10157-013-0789-5.PMC3775849.PMID23584881.
  17. ^Sands JM, Blount MA, Klein JD (2011)."Regulation of renal urea transport by vasopressin".Transactions of the American Clinical and Climatological Association.122:82–92.PMC3116377.PMID21686211.
  18. ^Knepper MA, Kim GH, Fernández-Llama P, Ecelbarger CA (March 1999)."Regulation of thick ascending limb transport by vasopressin".Journal of the American Society of Nephrology.10(3): 628–34.doi:10.1681/ASN.V103628.PMID10073614.
  19. ^Rieg T, Tang T, Uchida S, Hammond HK, Fenton RA, Vallon V (January 2013)."Adenylyl cyclase 6 enhances NKCC2 expression and mediates vasopressin-induced phosphorylation of NKCC2 and NCC".Am. J. Pathol.182(1): 96–106.doi:10.1016/j.ajpath.2012.09.014.PMC3532715.PMID23123217.
  20. ^Ares GR, Caceres PS, Ortiz PA (December 2011)."Molecular regulation of NKCC2 in the thick ascending limb".Am. J. Physiol. Renal Physiol.301(6): F1143–59.doi:10.1152/ajprenal.00396.2011.PMC3233874.PMID21900458.
  21. ^Forsling ML, Montgomery H, Halpin D, Windle RJ, Treacher DF (May 1998)."Daily patterns of secretion of neurohypophysial hormones in man: effect of age".Experimental Physiology.83(3): 409–18.doi:10.1113/expphysiol.1998.sp004124.PMID9639350.S2CID2295415.
  22. ^Magtanong E (2017)."What Is Nausea? A Historical Analysis of Changing Views".Auton Neurosci.202:5–17.doi:10.1016/j.autneu.2016.07.003.PMC5203950.PMID27450627.
  23. ^Wiltshire T, Maixner W, Diatchenko L (December 2011). "Relax, you won't feel the pain".Nature Neuroscience.14(12): 1496–7.doi:10.1038/nn.2987.PMID22119947.S2CID205434100.
  24. ^Dunlap JC (January 1999)."Molecular bases for circadian clocks".Cell.96(2): 271–90.doi:10.1016/s0092-8674(00)80566-8.PMID9988221.S2CID14991100.
  25. ^Jin X, Shearman LP, Weaver DR, Zylka MJ, de Vries GJ, Reppert SM (January 1999)."A molecular mechanism regulating rhythmic output from the suprachiasmatic circadian clock".Cell.96(1): 57–68.doi:10.1016/s0092-8674(00)80959-9.PMID9989497.S2CID6916996.
  26. ^Wang XM, Dayanithi G, Lemos JR, Nordmann JJ, Treistman SN (November 1991). "Calcium currents and peptide release from neurohypophysial terminals are inhibited by ethanol".The Journal of Pharmacology and Experimental Therapeutics.259(2): 705–11.PMID1941619.
  27. ^abMatsukawa T, Miyamoto T (March 2011). "Angiotensin II-stimulated secretion of arginine vasopressin is inhibited by atrial natriuretic peptide in humans".American Journal of Physiology. Regulatory, Integrative and Comparative Physiology.300(3): R624–9.doi:10.1152/ajpregu.00324.2010.PMID21123762.
  28. ^Collège des enseignants d'endocrinologie, diabète et maladie (2012-01-30).Endocrinologie, diabétologie et maladies métaboliques.Elsevier Masson.ISBN978-2-294-72233-2.
  29. ^Garrahy A, Thompston CJ (2019). "General Principles, Diabetes, Metabolism, Obesity, Gastrointestinal Hormones, Aging, Endocrine Toxicology".Encyclopedia of Endocrine Diseases.1(2): 969–974.
  30. ^Salata RA, Jarrett DB, Verbalis JG, Robinson AG (March 1988)."Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH".The Journal of Clinical Investigation.81(3): 766–74.doi:10.1172/JCI113382.PMC442524.PMID2830315.
  31. ^Day TA, Sibbald JR (June 1990). "Noxious somatic stimuli excite neurosecretory vasopressin cells via A1 cell group".The American Journal of Physiology.258(6 Pt 2): R1516-20.doi:10.1152/ajpregu.1990.258.6.R1516.PMID2360697.
  32. ^Höglund OV, Hagman R, Olsson K, Olsson U, Lagerstedt AS (October 2014). "Intraoperative changes in blood pressure, heart rate, plasma vasopressin, and urinary noradrenalin during elective ovariohysterectomy in dogs: repeatability at removal of the 1st and 2nd ovary".Veterinary Surgery.43(7): 852–9.doi:10.1111/j.1532-950X.2014.12264.x.PMID25130060.
  33. ^Goldmann A, Hoehne C, Fritz GA, Unger J, Ahlers O, Nachtigall I, et al. (September 2008). "Combined vs. Isoflurane/Fentanyl anesthesia for major abdominal surgery: Effects on hormones and hemodynamics".Medical Science Monitor.14(9): CR445-52.PMID18758414.
  34. ^Furuya K, Shimizu R, Hirabayashi Y, Ishii R, Fukuda H (May 1993)."Stress hormone responses to major intra-abdominal surgery during and immediately after sevoflurane-nitrous oxide anaesthesia in elderly patients".Canadian Journal of Anaesthesia.40(5 Pt 1): 435–9.doi:10.1007/BF03009513.PMID8390330.
  35. ^Haas M, Glick SM (May 1978). "Radioimmunoassayable plasma vasopressin associated with surgery".Archives of Surgery.113(5): 597–600.doi:10.1001/archsurg.1978.01370170059011.PMID646620.
  36. ^Nussey SS, Page SR, Ang VT, Jenkins JS (March 1988). "The response of plasma oxytocin to surgical stress".Clinical Endocrinology.28(3): 277–82.doi:10.1111/j.1365-2265.1988.tb01213.x.PMID3168310.S2CID37668345.
  37. ^Melville RJ, Forsling ML, Frizis HI, LeQuesne LP (December 1985). "Stimulus for vasopressin release during elective intra-abdominal operations".The British Journal of Surgery.72(12): 979–82.doi:10.1002/bjs.1800721215.PMID4084755.S2CID43764321.
  38. ^Moran WH, Miltenberger FW, Shuayb WA, Zimmermann B (July 1964). "The Relationship of Antidiuretic Hormone Secretion to Surgical Stress".Surgery.56:99–108.PMID14175989.
  39. ^Gutt CN, Oniu T, Mehrabi A, Schemmer P, Kashfi A, Kraus T, et al. (2004)."Circulatory and respiratory complications of carbon dioxide insufflation".Digestive Surgery.21(2): 95–105.doi:10.1159/000077038.PMID15010588.S2CID3369276.ProQuest223606053.
  40. ^Nguyen NT, Wolfe BM (February 2005)."The physiologic effects of pneumoperitoneum in the morbidly obese".Annals of Surgery.241(2): 219–226.doi:10.1097/01.sla.0000151791.93571.70.PMC1356906.PMID15650630.
  41. ^Alberts B, Bray D, Hopkin K, Johnson AD, Lewis J, Roberts K (2014).Essential Cell Biology.Garland Science.ISBN978-0-8153-4455-1.
  42. ^Bielsky IF, Hu SB, Szegda KL, Westphal H, Young LJ (March 2004)."Profound impairment in social recognition and reduction in anxiety-like behavior in vasopressin V1a receptor knockout mice".Neuropsychopharmacology.29(3): 483–93.doi:10.1038/sj.npp.1300360.PMID14647484.
  43. ^Wersinger SR, Caldwell HK, Martinez L, Gold P, Hu SB, Young WS (August 2007)."Vasopressin 1a receptor knockout mice have a subtle olfactory deficit but normal aggression".Genes, Brain and Behavior.6(6): 540–51.doi:10.1111/j.1601-183X.2006.00281.x.PMID17083331.S2CID29923520.
  44. ^Lolait SJ, Stewart LQ, Jessop DS, Young WS, O'Carroll AM (February 2007)."The hypothalamic-pituitary-adrenal axis response to stress in mice lacking functional vasopressin V1b receptors".Endocrinology.148(2): 849–56.doi:10.1210/en.2006-1309.PMC2040022.PMID17122081.
  45. ^Wersinger SR, Kelliher KR, Zufall F, Lolait SJ, O'Carroll AM, Young WS (December 2004)."Social motivation is reduced in vasopressin 1b receptor null mice despite normal performance in an olfactory discrimination task".Hormones and Behavior.46(5): 638–45.doi:10.1016/j.yhbeh.2004.07.004.PMID15555506.S2CID38444963.
  46. ^Kanwar S, Woodman RC, Poon MC, Murohara T, Lefer AM, Davenpeck KL, et al. (October 1995)."Desmopressin induces endothelial P-selectin expression and leukocyte rolling in postcapillary venules".Blood.86(7): 2760–6.doi:10.1182/blood.V86.7.2760.2760.PMID7545469.
  47. ^Kaufmann JE, Oksche A, Wollheim CB, Günther G, Rosenthal W, Vischer UM (July 2000)."Vasopressin-induced von Willebrand factor secretion from endothelial cells involves V2 receptors and cAMP".The Journal of Clinical Investigation.106(1): 107–16.doi:10.1172/JCI9516.PMC314363.PMID10880054.
  48. ^Burtis CA, Ashwood ER, Bruns DE (2012).Tietz Textbook of Clinical Chemistry and Molecular Diagnostics(5th ed.).Elsevier Health Sciences.p. 1833.ISBN978-1-4557-5942-2.
  49. ^Donaldson D (1994)."Polyuria and Disorders of Thirst".In Williams DL, Marks V (eds.).Scientific Foundations of Biochemistry in Clinical Practice(2nd ed.).Butterworth-Heinemann.pp. 76–102.doi:10.1016/B978-0-7506-0167-2.50010-8.ISBN978-0-7506-0167-2.
  50. ^Li C, Wang W, Summer SN, Westfall TD, Brooks DP, Falk S, et al. (February 2008)."Molecular mechanisms of antidiuretic effect of oxytocin".Journal of the American Society of Nephrology.19(2): 225–32.doi:10.1681/ASN.2007010029.PMC2396735.PMID18057218.
  51. ^Joo KW, Jeon US, Kim GH, Park J, Oh YK, Kim YS, et al. (October 2004). "Antidiuretic action of oxytocin is associated with increased urinary excretion of aquaporin-2".Nephrology, Dialysis, Transplantation.19(10): 2480–6.doi:10.1093/ndt/gfh413.PMID15280526.
  52. ^Acher R, Chauvet J (July 1995). "The neurohypophysial endocrine regulatory cascade: precursors, mediators, receptors, and effectors".Frontiers in Neuroendocrinology.16(3): 237–89.doi:10.1006/frne.1995.1009.PMID7556852.S2CID12739464.
  53. ^abcde"Vasopressin"(PDF).F.A. Davis Company. 2017.Retrieved2017-03-13.[dead link]
  54. ^Baum S, Nusbaum M (March 1971). "The control of gastrointestinal hemorrhage by selective mesenteric arterial infusion of vasopressin".Radiology.98(3): 497–505.doi:10.1148/98.3.497.PMID5101576.
  55. ^abVerbalis JG, Goldsmith SR, Greenberg A, Schrier RW, Sterns RH (November 2007). "Hyponatremia treatment guidelines 2007: expert panel recommendations".The American Journal of Medicine.120(11 Suppl 1): S1–21.CiteSeerX10.1.1.499.7585.doi:10.1016/j.amjmed.2007.09.001.PMID17981159.
  56. ^Young LJ (October 2009). "The neuroendocrinology of the social brain".Frontiers in Neuroendocrinology.30(4): 425–8.doi:10.1016/j.yfrne.2009.06.002.PMID19596026.S2CID31960688.
  57. ^Mavani GP, DeVita MV, Michelis MF (2015)."A review of the nonpressor and nonantidiuretic actions of the hormone vasopressin".Frontiers in Medicine.2:19.doi:10.3389/fmed.2015.00019.PMC4371647.PMID25853137.
  58. ^Iovino M, Messana T, De Pergola G, Iovino E, Dicuonzo F, Guastamacchia E, et al. (2018). "The Role of Neurohypophyseal Hormones Vasopressin and Oxytocin in Neuropsychiatric Disorders".Endocrine, Metabolic & Immune Disorders Drug Targets.18(4): 341–347.doi:10.2174/1871530318666180220104900.PMID29468985.S2CID3465601.

Further reading

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