Disease relevance of Avpr1a

• By blocking the vascular V1a receptors, it may compromise the patient's ability to maintain arterial blood pressure during hemorrhage [1].
• Experiments were performed to get insight into the role of AVP receptor V(1a) regulation with age, i.e., during development and maintenance of high blood pressure [2].
• Dehydration decreased expression approximately 50% in renal vessels independent of rat strain; water loading increased V1a mRNA [3].
• Chronic metabolic acidosis increased V1a receptor mRNA expression in the CD but decreased V2 receptor mRNA expression [4].
• The study provides evidence for significant changes of expression of AT1aR mRNA, V1aR mRNA and NOS1 mRNA in the specific brain regions of rats with the renovascular hypertension [5].

Psychiatry related information on Avpr1a

• Viral vector-mediated gene transfer of the vole V1a vasopressin receptor in the rat septum: improved social discrimination and active social behaviour [6].
• This study explores the effects of enhancing vasopressin V1a receptor expression in the septum using viral vector-mediated gene transfer on social discrimination and social interactions [6].
• In a social discrimination paradigm, only V1aR-AAV-treated animals succeeded in discriminating a previously encountered from a novel juvenile after an interexposure interval (IEI) of more than 2 h, demonstrating the functional incorporation of the vole V1a receptor in the rat septal circuits underlying short-term memory processes [6].
• Blocking the endogenous AVP by 25 or 1 microg of the V1a receptor antagonist d(CH(2))(5)[Tyr(Me)(2)]AVP (AAVP) before MPH treatment significantly augmented the motor activity in SO rats only and abolished the differences seen between SO and PE animals after MPH application [7].

High impact information on Avpr1a

• The liver cDNA encodes a protein with seven putative transmembrane domains, which binds arginine vasopressin and related compounds with affinities similar to the native rat V1a receptor [8].
• Molecular cloning and expression of a rat V1a arginine vasopressin receptor [8].
• We report here the cloning of a complementary DNA encoding the hepatic V1a arginine vasopressin receptor [8].
• Plasma membranes prepared from the inner medullae of CRF rats exhibit a marked decrease in apparent AVP receptor number but no change in the apparent number of beta adrenergic receptors [9].
• Thus, the two AVP receptor subtypes are distributed differently along the nephron, and these mRNAs are regulated differently in the dehydrated state [10].

Chemical compound and disease context of Avpr1a

• To investigate the mechanism underlying the deficits in social behavior induced by blockade of N-methyl-D-aspartate (NMDA) receptors, this study examined the effect of noncompetitive NMDA antagonists on AVP receptor binding and social interaction in the rat [11].
• Altered expression of angiotensin AT1a and vasopressin V1a receptors and nitric oxide synthase mRNA in the brain of rats with renovascular hypertension [5].
• The present study examined the effect of streptozotocin-induced diabetes mellitus in rats on the [Ca2+]i of the renal proximal tubular cells and on their mRNAs of the PTH-PTHrP, V1a and AT1 receptors [12].
• The role of arginine-vasopressin (AVP) in the pathogenesis of deoxycorticosterone acetate (DOCA) salt hypertension in rats was studied with AVP receptor antagonists for its tubular (V2) and/or vascular (V1) actions [13].
• We previously reported that the number of renal AVP receptors decreased in rats with diabetes insipidus which were treated with lithium, suggesting that the change in the AVP receptor is a primary cause of polyuric state induced by lithium [14].

Biological context of Avpr1a

• Arginine vasopressin receptors are G protein-coupled and have been divided into at least three types; the V1a (vascular/hepatic) and V1b (anterior pituitary) receptors which act through phosphatidylinositol hydrolysis to mobilize intracellular Ca2+, and the V2 (kidney) receptor which is coupled to adenylate cyclase [8].
• In this study, microlocalization of mRNA coding for V1a and V2 receptors was carried out in the rat kidney using a reverse transcription and polymerase chain reaction [10].
• This study suggests that the vasoconstrictor action of AVP within the renal medulla is mediated through the V1aR and that the modulatory V2R-mediated vasodilation is probably through the release of paracrine hormones found within the renal interstitial or tubular cells [15].
• Exaggerated arginine vasopressin (AVP)-induced calcium signaling and renal vasoconstriction, characteristic in young spontaneously hypertensive rats (SHR) during euvolemia, are related to greater amounts of V1a receptor mRNA and V1a protein in preglomerular resistance arterioles [3].
• The present study determined whether V1a receptor density and calcium signal transduction in the renal vasculature of young SHR is regulated appropriately during physiological changes in hydration state [3].

Anatomical context of Avpr1a

• V1a-R were localized mainly in globose basal cells and at the apical side of the epithelium, in the area of the dendritic knobs of OSNs [16].
• PCR product of the V2 receptor mRNA was detected in the hippocampus, but that of V1a receptor mRNA was not [17].
• OBJECTIVE: The objective of the study was to determine in the rat model whether the uterotonic action of vasopressin is mediated by the vasopressin V1a receptor in the uterus, by the oxytocin receptor, or by both [1].
• Cellular expression of V1a vasopressin receptor mRNA in the female rat preoptic area: effects of oestrogen [18].
• At present, the distribution of the V1aR and V2R within the renal cortical and medullary microcirculation has not been determined [15].

Associations of Avpr1a with chemical compounds

• Moreover, when Tyr115 is replaced by an Asp and a Phe, the amino acids naturally occurring in the V2 and in the OT receptor subtypes, the agonist selectivity of the V1a receptor switches accordingly [19].
• Arginine-vasopressin (AVP) in the septum and hippocampus are thought to be involved in memory and learning, and their receptors have been classified into three subtypes, V1a, V1b and V2 [17].
• Previous studies have demonstrated that both the V2-receptor agonist, 1-desamino-8-D-arginine vasopressin (dDAVP), and the V1a-receptor agonist, [Phe2, Orn8]vasotocin (PO-VT), increase intracellular calcium concentration ([Ca2+]i) in the rat inner medullary collecting duct (IMCD) [20].
• Pretreating VSMCs with chloroquine prevented AVP receptor recycling, indicating that the AVP-receptor complex requires endosomal processing [21].
• The motor actions of centrally injected AVP, as well as septal AVP receptor characteristics (number and affinity), and AVP-stimulated phosphoinositide (PI) hydrolysis were then investigated in long-term castrated and sham control rats [22].

Physical interactions of Avpr1a

• Comparative effects of loop diuretics on AVP-receptor binding and AVP-sensitive adenylate cyclase activity [23].
• Competition studies with various OT and AVP receptor agonists and antagonists confirmed that the binding was to OT receptors [24].
• Results of vasopressin V1A receptor binding kinetics and plasma renin or aldosterone concentrations did not suggest a lasting effect of OPC-21268 on the vasopressin system or of ramipril on the renin-angiotensin system following treatment withdrawal.(ABSTRACT TRUNCATED AT 250 WORDS)[25]

Regulatory relationships of Avpr1a

• Antagonists for oxytocin ([des-glycinamide9,d(CH2)5(1),O-Me-Tyr2,Thr4,Orn8]vaso tocin), V2 ([d(CH2)5(1),D-Ile2,Ile4,Arg8]vasopressin), and V1a ([d(CH2)5(1),O-Me-Tyr2,Arg8]vasopressin) receptors partially inhibited the [Ca2+]i response induced by 10 nM AVP (89.5, 81.6, and 51.4% inhibition, respectively) [26].
• AVP (n = 9) and OT (n = 8) induced increases in [Ca2+]i were completely blocked by the V1A-receptor antagonist d(CH2)5Tyr(Me)2AVP [27].

Other interactions of Avpr1a

• Recent studies have revealed that arginine vasopressin (AVP) has at least two types of receptors in the kidney: V1a receptor and V2 receptor [10].
• This vasopressin receptor is distinct from both the V1a receptor and the V2 receptor and may be either the V1b receptor or a novel vasopressin receptor subtype [26].
• A nonselective oxytocin-V1a receptor antagonist, a selective oxytocin receptor antagonist, and a selective V1a receptor antagonist were selected for this study [1].
• A single clone, encoding a functional AVP receptor corresponding to the V1a subtype was finally characterized as a G protein-coupled receptor [28].
• The transcript encoding VACM-1, a novel AVP receptor, appears to be ubiquitously expressed in various tissues of the laboratory rat [29].

Analytical, diagnostic and therapeutic context of Avpr1a

• Large signals for V1a receptor PCR product were detected in the glomerulus, initial cortical collecting duct, cortical collecting duct, outer medullary collecting duct, inner medullary collecting duct, and arcuate artery [10].
• The cell response was essentially ascribed to the V1a AVP receptor, whose presence was confirmed by RT-PCR and immunolabelling [16].
• These observations may be more general, as autoradiography revealed similar lobular distributions of V1a receptors and alpha1 adrenergic receptors; the amounts of both were greatest in hepatocytes surrounding central veins [30].
• Multiple immunocytochemical labeling combined with confocal microscopy allowed the identification of the V1a-labeled cells as gonadotropes [31].
• In this study, we investigated the effects of chronic adrenalectomy (ADX) and subsequent treatment with supraphysiological doses of corticosterone (B) on the gene expression of AVP receptors of the V1a subtype in the septum, hippocampus and hypothalamic arcuate (ARC) nucleus using semiquantitative in situ hybridization histochemistry [32].

References