Vasopressin receptor 1B

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Vasopressin V1b receptor (V1BR) also known as vasopressin 3 receptor (VPR3) or antidiuretic hormone receptor 1B is a protein that in humans is encoded by the AVPR1B (arginine vasopressin receptor 1B) gene.

V1BR acts as a receptor for vasopressin. AVPR1B belongs to the subfamily of G-protein coupled receptors. Its activity is mediated by G proteins which stimulate a phosphatidylinositol-calcium second messenger system.It is a major contributor to homeostasis and the control of water, glucose, and salts in the blood. Arginine vasopressin has four receptors, each of which are located in different tissues and have specific functions. AVPR1b is a g-protein coupled pituitary receptor that has only recently been characterized because of its rarity.[1]

It has been found that the 420-amino-acid sequence of the AVPR1B receptor shared the most overall similarities with the AVP1A, AVP2 and oxytocin receptors.[2] AVPR1B maps to chromosome region 1q32 and is a member of the vasopressin/oxytocin family subfamily.[3]

Tissue distribution

AVPR1B was initially described as a novel vasopressin receptor located in the anterior pituitary, where it stimulates ACTH release.[4] Subsequent studies have shown that it is also present in the brain.[5][6]

Clinical significance

Behavioral

Inactivation of the Avpr1b gene in mice (knockout) produces mice with greatly reduced aggression and a reduced ability to recognize recently investigated mice.[7] Defensive behaviour and predatory behaviours appear normal in these knockout mice,[8] but there is evidence that social motivation or awareness is reduced.[9] The AVPR1B antagonist, SSR149415, has been shown to have anti-aggressive actions in hamsters[10] and anti-depressant- and anxiety (anxiolytic)-like behaviors in rats.[11] A single nucleotide polymorphism (SNP) has been associated with susceptibility to depression in man.[2]

Metabolic

Various stress-induced elevations of ACTH are blunted in the Avpr1b knockout mouse.[12]

Oncology

AVPR1B is expressed at high levels in ACTH-secreting pituitary adenomas as well as in bronchial carcinoids[13] responsible for the ectopic ACTH syndrome.[14]

Ligands

Nelivaptan (SSR149415)[15] and D-[Leu4-Lys8]-vasopressin[16] are a specific antagonist and agonist for the vasopressin 1b receptor, respectively.

Function

AVPR1B is found in different parts of the body and thus has several influences and regulatory actions. Arginine vasopressin influences several symptoms related to affective disorders including significant memory processes, pain sensitivity, synchronization of biological rhythms and the timing and quality of REM sleep.[2] Studies have shown that AVPR1B deficiencies produce behavioral changes that can be reversed when the peptide is replaced.[2] These effects are expressed through contact with specific plasma membrane receptors.[2] AVPR1B is responsible for fueling the effects of vasopressin on ACTH release.[3] This interaction takes place as Arginine Vasopressin works with corticotropin releasing hormone to stimulate the pituitary gland to secrete ACTH.[2] AVPR1b is then responsible for mediating the stimulatory effect of vasopressin on ACTH release. Several G proteins are also involved in the signal transduction pathways linked with AVPR1B.[1] These relationships depend on the level of receptor expression and concentration of vasopressin.[1] For example, AVPR1B causes secretion of ACTH from the anterior pituitary cells in a dose-dependent relationship by activating protein kinase C via the Gq/11 protein.[1]

Application

There have been several experiments which have studied these interactions further and revealed AVPR1B’s role in psychological disorders and regulatory functions. Halotypes of AVPR1B are associated with increased protective effects to recurrent major depression.[2] AVPR1B has also been associated with higher cortisol responses to psychosocial stress in children with psychiatric disorders compared with carriers of glucocorticoid receptor gene.[17] AVPR1b has also shown involvement in regulation of brain water content and cerebral edema.[18] This was revealed as increased levels of AVPR1B mRNA on the choroid plexus were discovered as a result of increased plasma osmolality.[18] The increase after a reduction of brain water content from salt water loading indicated AVPR1B’s role in the neuroendocrine feedback loop in maintaining normal central nervous system fluid balance.[18]

References

  1. ↑ 1.0 1.1 1.2 1.3 Holmes CL, Landry DW, Granton JT (December 2003). "Science review: Vasopressin and the cardiovascular system part 1--receptor physiology". Crit Care. 7 (6): 427–34. doi:10.1186/cc2337. PMC 374366. PMID 14624682.
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 van West D, Del-Favero J, Aulchenko Y, Oswald P, Souery D, Forsgren T, Sluijs S, Bel-Kacem S, Adolfsson R, Mendlewicz J, Van Duijn C, Deboutte D, Van Broeckhoven C, Claes S (March 2004). "A major SNP haplotype of the arginine vasopressin 1B receptor protects against recurrent major depression". Mol. Psychiatry. 9 (3): 287–92. doi:10.1038/sj.mp.4001420. PMID 15094789.
  3. ↑ 3.0 3.1 "anti-Arginine Vasopressin Receptor 1B (AVPR1B) antibody (ABIN122463)". antibodies-online.
  4. ↑ Antoni FA, Holmes MC, Makara GB, Kárteszi M, László FA (1984). "Evidence that the effects of arginine-8-vasopressin (AVP) on pituitary corticotropin (ACTH) release are mediated by a novel type of receptor". Peptides. 5 (3): 519–22. doi:10.1016/0196-9781(84)90080-9. PMID 6089144.
  5. ↑ Hernando F, Schoots O, Lolait SJ, Burbach JP (2001). "Immunohistochemical localization of the vasopressin V1b receptor in the rat brain and pituitary gland: anatomical support for its involvement in the central effects of vasopressin". Endocrinology. 142 (4): 1659–68. doi:10.1210/en.142.4.1659. PMID 11250948.
  6. ↑ Young WS, Li J, Wersinger SR, Palkovits M (2006). "The Vasopressin 1b Receptor is Prominent in the Hippocampal Area CA2 Where It Is Unaffected by Restraint Stress or Adrenalectomy". Neuroscience. 143 (4): 1031–9. doi:10.1016/j.neuroscience.2006.08.040. PMC 1748954. PMID 17027167.
  7. ↑ Wersinger SR, Ginns EI, O'Carroll AM, Lolait SJ, Young WS (2002). "AVPR1B knockout reduces aggressive behavior in male mice". Mol. Psychiatry. 7 (9): 975–84. doi:10.1038/sj.mp.4001195. PMID 12399951.
  8. ↑ Wersinger SR, Caldwell HK, Christiansen M, Young WS (2007). "Disruption of the Vasopressin 1b Receptor Gene Impairs the Attack Component of Aggressive Behavior in Mice". Genes, Brain and Behavior. 6 (7): 653–60. doi:10.1111/j.1601-183X.2006.00294.x. PMC 2486432. PMID 17284170.
  9. ↑ Wersinger SR, Kelliher KR, Zufall F, Lolait SJ, O'Carroll AM, Young WS (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. PMID 15555506.
  10. ↑ Blanchard RJ, Griebel G, Farrokhi C, Markham C, Yang M, Blanchard DC (2005). "AVP V1b selective antagonist SSR149415 blocks aggressive behaviors in hamsters". Pharmacol. Biochem. Behav. 80 (1): 189–94. doi:10.1016/j.pbb.2004.10.024. PMID 15652395.
  11. ↑ Serradeil-Le Gal C, Wagnon J, Tonnerre B, Roux R, Garcia G, Griebel G, Aulombard A (2005). "An overview of SSR149415, a selective nonpeptide vasopressin V1b receptor antagonist for the treatment of stress-related disorders". CNS Drug Reviews. 11 (1): 53–68. doi:10.1111/j.1527-3458.2005.tb00035.x. PMID 15867952.
  12. ↑ Lolait SJ, Stewart LQ, Jessop DS, Young WS, O'Carroll AM (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. PMC 2040022. PMID 17122081.
  13. ↑ Arlt W, Dahia PL, Callies F, Nordmeyer JP, Allolio B, Grossman AB, Reincke M (1997). "Ectopic ACTH production by a bronchial carcinoid tumour responsive to desmopressin in vivo and in vitro". Clin. Endocrinol. 47 (5): 623–7. doi:10.1046/j.1365-2265.1997.3091129.x. PMID 9425403.
  14. ↑ de Keyzer Y, Lenne F, Auzan C, Jégou S, René P, Vaudry H, Kuhn JM, Luton JP, Clauser E, Bertagna X (1996). "The pituitary V3 vasopressin receptor and the corticotroph phenotype in ectopic ACTH syndrome". J. Clin. Invest. 97 (5): 1311–8. doi:10.1172/JCI118547. PMC 507185. PMID 8636444.
  15. ↑ Serradeil-Le Gal C, Wagnon J, Simiand J, Griebel G, Lacour C, Guillon G, Barberis C, Brossard G, Soubrié P, Nisato D, Pascal M, Pruss R, Scatton B, Maffrand JP, Le Fur G (2002). "Characterization of (2S,4R)-1-[5-chloro-1-[(2,4-dimethoxyphenyl)sulfonyl]-3-(2-methoxy-phenyl)-2-oxo-2,3-dihydro-1H-indol-3-yl]-4-hydroxy-N,N-dimethyl-2-pyrrolidine carboxamide (SSR149415), a selective and orally active vasopressin V1b receptor antagonist". J. Pharmacol. Exp. Ther. 300 (3): 1122–30. doi:10.1124/jpet.300.3.1122. PMID 11861823.
  16. ↑ Pena A, Murat B, Trueba M, Ventura MA, Bertrand G, Cheng LL, Stoev S, Szeto HH, Wo N, Brossard G, Serradeil-Le Gal C, Manning M, Guillon G (2007). "Pharmacological and physiological characterization of d[Leu4, Lys8]vasopressin, the first V1b-selective agonist for rat vasopressin/oxytocin receptors". Endocrinology. 148 (9): 4136–46. doi:10.1210/en.2006-1633. PMID 17495006.
  17. ↑ van West D, Del-Favero J, Deboutte D, Van Broeckhoven C, Claes S (August 2010). "Associations between common arginine vasopressin 1b receptor and glucocorticoid receptor gene variants and HPA axis responses to psychosocial stress in a child psychiatric population". Psychiatry Res. 179 (1): 64–8. doi:10.1016/j.psychres.2009.04.002. PMID 20472303.
  18. ↑ 18.0 18.1 18.2 Zemo DA, McCabe JT (2001). "Salt-loading increases vasopressin and vasopressin 1b receptor mRNA in the hypothalamus and choroid plexus". Neuropeptides. 35 (3–4): 181–8. doi:10.1054/npep.2001.0864. PMID 11884209.

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