Disease relevance of Avpr2

• These findings provide evidence that chronic stimulation of vasopressin V2 receptor raises basal blood pressure in rats and exacerbates the development of DOCA-salt hypertension, organ damage, and mortality [1].
• BSC1 inhibition complements effects of vasopressin V2 receptor antagonist on hyponatremia in SIADH rats [2].
• However, OPC-31260 (21.6 mumol/kg IV), a vasopressin V2-receptor antagonist, attenuated both the hypotensive and bradycardic responses to hemorrhage in Long-Evans rats [3].
• In the Brattleboro rat with diabetes insipidus vasopressin V2 receptor mRNA and the mRNA of various adenylyl cyclase (AC) isoforms are moderately reduced compared with those of normal rats [4].
• These results suggest that dual vasopressin V1A and V2 receptor antagonists provide greater benefit than selective vasopressin V2 receptor antagonists in the treatment of congestive heart failure [5].

High impact information on Avpr2

• Rat renal arcade segment expresses vasopressin-regulated water channel and vasopressin V2 receptor [6].
• To examine whether expression and distribution of aquaporin of collecting duct (AQP-CD) are regulated by vasopressin V2 receptor (V2R), we performed immunohistochemical studies with specific antibody against AQP-CD [7].
• Expression and distribution of aquaporin of collecting duct are regulated by vasopressin V2 receptor in rat kidney [7].
• One group of nephrotic rats received a vasopressin V2 receptor blocker (V2X) from 4 to 16 wk after injection of adriamycin, whereas a second group received no treatment (NoRx) [8].
• The vasopressin V2 receptor agonist 1-desamino-8-D-arginine vasopressin (dDAVP) resulted in a significant increase of 32% in renal medullary interstitial [NO] [9].

Chemical compound and disease context of Avpr2

• DDAVP, a vasopressin V2-receptor agonist (0.19 pmol/kg per minute for 24 hours), did not affect the cardiovascular responses to hemorrhage in Brattleboro rats, although it maintained urine production within normal limits [3].

Biological context of Avpr2

• Downregulation of renal vasopressin V2 receptor and aquaporin-2 expression parallels age-associated defects in urine concentration [10].
• Infusion of desmopressin (1-1000 ng/kg per min, i.r.a.), a vasopressin V2 receptor-selective agonist, failed to induce renal vasodilation or vasoconstriction [11].
• The constriction depends on activation of smooth muscle vasopressin V1A receptors and is modulated by endothelial nitric oxide but not by prostacyclin or vasopressin V2 receptor-related vasodilation [12].
• Vasopressin induces dopamine release and cyclic AMP efflux from the brain of water-deprived rats: inhibitory effect of vasopressin V2 receptor-mediated phosphorylation [13].
• In contrast, neither ANP-B nor vasopressin V2 receptor gene expression was detected [14].

Anatomical context of Avpr2

• Evidence for the existence of vasopressin V2 receptor mRNA in rat hippocampus [15].
• beta2-adrenergic but not vasopressin V2 receptor mRNAs are expressed in the stria vascularis of the rat inner ear [16].
• In addition, the vasopressin V2-receptor agonist 1-desamino-8-D-arginine vasopressin had no effect on the Na(+)-Ca2+ exchanger in rat brain synaptosomes [17].

Associations of Avpr2 with chemical compounds

• To prove the role of the vasopressin V2 receptor (V2R) in the regulation of intracellular AQP-2 shuttling, we examined the acute effects of vasopressin and V2R antagonist on the distribution of AQP-2 in the cells [18].
• Nitric oxide, but not vasopressin V2 receptor-mediated vasodilation, modulates vasopressin-induced renal vasoconstriction in rats [11].
• The present study demonstrates for the first time that desmopressin relaxant effect is antagonized by the vasopressin V2 receptor antagonist SR121463A, but also by the vasopressin V1A receptor antagonist SR49059, suggesting that desmopressin-induced relaxation is mediated by a receptor subtype sharing both V1A and V2 pharmacological profiles [19].
• The potentiation by vasopressin was reduced by the antagonist of vasopressin V1 receptors d(CH2)5Tyr(Me)AVP (10(-7) M), but not by the vasopressin V2 receptor antagonist d(CH2)5D-Ile2, Ile4AVP (10(-7) M) [20].
• Doses of noradrenaline from 40 to 160 ng.kg-1 had similar pressor effects in the treated and control rats, while the pressor response to the highest dose of noradrenaline (320 ng.kg-1) was significantly lower (P < 0.01) in the vasopressin V2 receptor agonist-treated rats [21].

Regulatory relationships of Avpr2

• It is known that vasopressin V2 receptor (V2R) mRNA is downregulated by elevated plasma arginine vasopressin (AVP) following chronic osmotic stimulation [22].
• The present results indicate that the distribution and amount of AQP-CD in the CD cells are regulated by vasopressin V2 receptor [7].

Other interactions of Avpr2

• Expression of smooth muscle alpha-actin was specific to the descending vasa recta and not a result of tubular contamination because RT-PCR amplification of the vasopressin V2 receptor, which is a specific tubular marker, did not occur [23].
• Studies have also shown that the vasopressin V2 receptor (V2R) may modulate AVP-mediated vasoconstriction [24].
• [Mpa1,D-Arg8]Vasopressin (desmopressin; 0.1-100 nM), or vasopressin (0.01-1 nM) after blockade of the vasopressin V1A receptor by SR 49059, induced no vasopressin V2 receptor-related renal relaxation in kidneys with vascular tone previously restored by noradrenaline or prostaglandin F2 alpha [12].
• Previous in vitro microperfusion studies showed that oxytocin has an antidiuretic action, most likely mediated by the vasopressin V2 receptor (V2R) in rat IMCD [25].
• The antidiuretic action of senktide was blocked by pretreatment with the vasopressin V2 receptor antagonist OPC-31260 (1 mg/kg, i.v.), but not by microinjection of the angiotensin II AT-1 receptor antagonist losartan (1 nmol) into the PVN [26].

References