Disease relevance of Avp

• In contrast, heterozygous mice expressing a mutation that truncates the AVP precursor (C67X) exhibited polyuria and polydipsia by 2 months of age and these features of DI progressively worsened with age [1].
• Familial neurohypophyseal diabetes insipidus (FNDI) is an autosomal dominant disorder caused by mutations in the arginine vasopressin (AVP) precursor [1].
• In conclusion, the majority of transgenic mice for AVP/large T-antigen develop pituitary tumors originating in and composed of somatotrophs [2].
• AVP/SV40 transgenic mice provide a unique experimental model for somatotroph tumors that are neither preceded by, nor associated with somatotroph hyperplasia [2].
• In the hypothalamus, restorative gene therapy has been successfully implemented in Brattleboro rats, an arginine vasopressin (AVP) mutant which suffers from diabetes insipidus, and in Koletsky (fa(k)/fa(k)) and in Zucker (fa/fa) rats which have leptin receptor mutations that render them obese, hyperphagic and hyperinsulinemic [3].

Psychiatry related information on Avp

• Neither arginine vasopressin nor alpha-melanocyte stimulating hormone changed parameters of exploratory and social behaviors, strengthening the possibility that their roles in increasing acquisition and retention of operant tasks are specific to neural mechanisms involved in memory and learning [4].
• Transepithelial Pf was measured in microdissected IMCDs after 18-48 h of water deprivation and in the presence of 0.1 nM arginine vasopressin (to make basolateral Pf rate limiting) [5].
• Lack of the development of morphine tolerance in experimental amnesia: role of arginine vasopressin [6].
• The authors discuss AVP as a possible mechanism by which early experience shapes adult paternal behavior [7].
• To examine a non-specific behavioral action of the peptide, the effect of AVP treatment on locomotor activity was assessed [8].

High impact information on Avp

• Arginine vasopressin influences male reproductive and social behaviours in several vertebrate taxa through its actions at the V1a receptor in the brain [9].
• Arginine vasopressin maintains ethanol tolerance [10].
• Both monokines stimulated pituitary cells (AtT-20) to release adrenocorticotropic hormone; interleukin-1 was equipotent with a combination of corticotropin-releasing factor and arginine vasopressin, and hepatocyte-stimulating factor was at least three times as effective [11].
• Body fluid homeostasis requires the release of arginine-vasopressin (AVP, an antidiuretic hormone) from the neurohypophysis [12].
• A mutation in the AVP signal sequence [A(-1)T] is associated with a relatively mild phenotype or delayed presentation in humans [1].

Chemical compound and disease context of Avp

• Familial neurohypophyseal diabetes insipidus (FNDI) in humans is an autosomal dominant disorder caused by a variety of mutations in the arginine vasopressin (AVP) precursor [13].
• In the glia-targeted mice, blood pressure could be corrected by intracerebroventricular injection of the Ang-II type 1 receptor antagonist losartan, and intravenous injection of a ganglion blocking agent, but not an arginine vasopressin V1 receptor antagonist, lowered blood pressure [14].
• NC-1900, an active fragment analog of arginine vasopressin [arginine vasopressin-(4-9)], has proved to be capable of improving the spatial memory deficits and the impairments in passive avoidance test [15].
• The peptide Z-Pro-Leu-Gly-NH2 attenuated puromycin-induced amnesia in mice when administered 5 days prior to training, while arginine vasopressin, lysine vasopressin and cyclo(Leu-Gly), were effective when given 24 hr before training [16].
• Neuroprotective effect of vasopressin analogues, arginine Vasopressin (AVP) and lysine Vasopressin (LVP) was evaluated against MgCl2 induced cerebral ischemia model [17].

Biological context of Avp

• Interspecific backcross analysis has now been used to map the Avp/Oxt complex to chromosome 2 in the mouse [18].
• Although AVP is used clinically as a potent vasoconstrictor (V1a receptor-mediated) in patients with circulatory shock, the physiological role of vasopressin V1a receptors in blood pressure (BP) homeostasis is ill-defined [19].
• AVP is involved in fluid homeostasis, while OXT is involved in lactation and parturition [18].
• AVP binding sites were mainly detected in the olfactory bulb and throughout the cerebral cortex [20].
• Similar genotype differences in the effects of estrogen on the numbers of OT- and AVP-containing cells were found in immunocytochemical studies performed in a separate set of mice [21].

Anatomical context of Avp

• AVP-induced vasopressor responses were abolished in the mutant mice; rather, AVP caused a decrease in BP, which occurred in part through V2 receptor-mediated release of nitric oxide from the vascular endothelium [19].
• AVP messenger RNA expression was increased in the paraventricular nucleus of Crhr1-/- mutants together with a marked increase in AVP-like immunoreactivity in the median eminence [22].
• The AVP replacement did not stimulate DNA synthesis in the target lymphocytes [23].
• These data indicate developmental changes in the steroidogenic responsiveness of Leydig cells to neurohypophysial hormones and suggest that AVP receptors might be under a regulatory mechanism(s) during puberty [24].
• These data suggest that PGE(2) modulates urine concentration by acting at EP(1) receptors, not in the collecting duct, but within the hypothalamus to promote AVP synthesis in response to acute WD [25].

Associations of Avp with chemical compounds

• To investigate the role of Avp in the hypothalamic-pituitary-adrenal axis response to stress, we measured plasma ACTH and corticosterone (CORT) levels in Avpr1b knockout (KO) mice and wild-type controls in response to two acute (restraint and insulin administration) and one form of chronic (daily restraint for 14 d) stress [26].
• Developmental changes in arginine vasopressin receptors and testosterone stimulation in Leydig cells [24].
• The AVP RIA can detect as little as 2 pg hormone and shows essentially no cross-reactivity with AVT or OT [27].
• The chicken pineal also contained AVT (about 300 pg/gland) and lacked AVP and OT [27].
• Cycloheximide totally abolished the AVP stimulation, suggesting that the AVP effect is dependent upon new protein synthesis [24].

Physical interactions of Avp

• Arginine vasopressin (AVP) regulates biological processes by binding to G protein-coupled receptors [28].

Regulatory relationships of Avp

• Interval mapping on chromosome 7 reveals substantial overlap between QTL that control AVP and Crf-R1 transcript abundance and on chromosome 12 for QTL that control CRF and Crf-R1, which may indicate loci that coordinate regulation of the CRF system [29].
• Our studies suggest that, at the hypothalamic level, CRH synthesis is the major target for feedback control by the GR and that transcriptional control of AVP and neurophysin plays only a supportive role in this process [30].
• Here we report, for the first time, that AVP specifically inhibits expression of the cyclin D1 gene, leading to cell cycle blockage and halting cell proliferation [31].
• Thus, AVP and FGF2 concur to activate ERK1/2 by different regulatory pathways [31].
• Arginine vasopressin induces the expression of c-fos in the mouse septum and hippocampus [32].

Other interactions of Avp

• Arginine-vasopressin (AVP) is a hormone that is essential for both osmotic and cardiovascular homeostasis, and exerts important physiological regulation through three distinct receptors, V1a, V1b, and V2 [19].
• Basal plasma AVP concentrations were significantly elevated in Crhr1-/- mice [22].
• In situ hybridization histochemistry revealed that estrogen treatment resulted in a significant increase in OT transcripts (151.6+/-6.0%) and a decrease in AVP transcripts (77.8+/-5.2%) in the PVN of WT mice, compared to the placebo control group [21].
• Hypertonicity regulates the aquaporin-2 promoter independently of arginine vasopressin [33].
• There was no additive effect of ET-1 and AVP on [Ca2+]i when they were added together [34].

Analytical, diagnostic and therapeutic context of Avp

• This deficit could be traced back to a blunted induction of hypothalamic AVP mRNA expression in WD EP(1)(-/-) mice as determined by quantitative RT-PCR [25].
• The determination of NO-synthesizing neurons was performed by double immunohistochemistry for the neuronal form of NO synthase (NOS), and AVP or OT [35].
• In the present study, we examined the effects of salt loading (drinking 2% NaCl for 5 days) on the expression of the AVP gene in the paraventricular (PVN) and supraoptic nuclei (SON) of wild-type, OTKO and heterozygous littermates using in situ hybridization histochemistry [36].
• None of the antagonists used blocked AVP-induced analgesia [37].
• After hypophysectomy, both AVP- and OXT-immunoreactive neurons showed an intense stainability 10 days after the operation regardless of ages [38].

References