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1  lack of agonist activity at the vasopressin V2 receptor.
2 orter to a greater extent than the wild type V2 receptor.
3 imately 30-fold reduced binding to the human V2 receptor.
4 e trafficking of the coexpressed full-length V2 receptor.
5 nt intracellular domains between the V1a and V2 receptors.
6 anging the C-terminal tails of the beta2 and V2 receptors.
7 oteins representing normal V1b receptors and V2 receptors.
8 renergic receptors, but not the vasopressin (V2) receptor.
9 tion by activating renal vasopressin type 2 (V2) receptors.
10 tributed throughout the cytosol, whereas the V2 receptor accumulated in a large aggregation of vesicl
11 ecretion (PDE3), and response to vasopressin V2 receptor activation (both).
12                                    Selective V2 receptor agonism is required for anti-DI activity and
13 on of S126 NKCC2 and T58 NCC, induced by the V2 receptor agonist (1-desamino-8-D-arginine vasopressin
14       METx forms nanofibers and is a partial V2 receptor agonist (determined by measuring MDCK cell l
15                                          The V2 receptor agonist 1-deamino-8-d-arginine vasopressin i
16 in/3-isobutyl-1-methylxanthine (IBMX) or the V2 receptor agonist [deamino-Cys(1),d-Arg(8)]vasopressin
17 labeling of both isoforms in response to the V2 receptor agonist [deamino-Cys1,D-Arg8]vasopressin (DD
18  peptide - METx - is a selective competitive V2 receptor agonist and an anti-diuretic.
19 xed vasopressin type 1a receptor/vasopressin V2 receptor agonist arginine vasopressin because of its
20 f selepressin with the selective vasopressin V2 receptor agonist desmopressin were similarly investig
21        1-Deamino-8-D-arginine vasopressin (a V2 receptor agonist, 0.1 nM) simulated the effects of AV
22 sought to examine the effects of vasopressin V2 receptor antagonism with tolvaptan on the changes in
23 erent drug type or combination (balanced V1a/V2 receptor antagonism) may be warranted.
24  duct responsiveness to an oral, nonpeptide, V2 receptor antagonist (VPA-985) in patients with chroni
25  effects of the oral, non-peptide, selective V2 receptor antagonist lixivaptan in 42 diuretic-requiri
26 ated with heart failure and suggest that the V2 receptor antagonist lixivaptan may be a promising the
27     Utilizing this protocol, the vasopressin V2 receptor antagonist precursor has been synthesized ea
28 re blocked by treatment with the vasopressin V2 receptor antagonist SR121463B, but not by treatment w
29                                          The V2 receptor antagonist tolvaptan is prescribed to patien
30  and after administration of the vasopressin V2 receptor antagonist tolvaptan.
31 tion is inhibited by the administration of a V2 receptor antagonist.
32 1061), a novel, oral, nonpeptide vasopressin V2-receptor antagonist in patients with chronic heart fa
33  long-term administration of the vasopressin V2-receptor antagonist tolvaptan (30 mg/day) on reducing
34 rance, >/=60 ml per minute), the vasopressin V2-receptor antagonist tolvaptan slowed the growth in to
35 , an oral, nonpeptide, selective vasopressin V2-receptor antagonist, shows promise in this condition.
36 hyponatremia, tolvaptan, an oral vasopressin V2-receptor antagonist, was effective in increasing seru
37 ovide further support for clinical trials of V2 receptor antagonists in PKD.
38                   Arginine vasopressin (AVP) V2 receptor antagonists inhibit cystogenesis in animal m
39 lications on the emerging use of vasopressin V2 receptor antagonists such as tolvaptan as safe and ef
40 f renal intracellular cAMP using vasopressin V2 receptor antagonists, and somatostatin analogues, as
41 e loop diuretics and salt tablets, urea, and V2 receptor antagonists.
42            Vaptans acting on the vasopressin V2 receptors (aquaretics) have attracted attention as a
43  study was to examine the renal effects of a V2 receptor arginine vasopressin (AVP) antagonist in hea
44 m responsiveness of the collecting duct to a V2 receptor AVP antagonist in chronic heart failure.
45                                  Vasopressin V2 receptor (AVPR2) mRNA was decreased 3 hours after UUO
46 d most often by mutations in the vasopressin V2 receptor (AVPR2).
47  between GH-releasing hormone (GHRH) and the V2 receptor-binding region of gp120, we initiated experi
48                                              V2 receptor blockade did not preserve renal function or
49                                              V2 receptor blockade increased urine volume without affe
50 oup of nephrotic rats received a vasopressin V2 receptor blocker (V2X) from 4 to 16 wk after injectio
51                     Tolvaptan, a vasopressin V2 receptor blocker, shows promise for management of hea
52 r1 upon its interaction with the vasopressin V2 receptor C-terminal phosphopeptide (V2Rpp).
53             Rare activating mutations of the V2 receptor can also cause SIAD.
54 interfere with the activity of the wild-type V2 receptor coexpressed in COS-7 cells.
55 o generate a yeast library expressing mutant V2 receptors containing mutations within the second intr
56 mal (and probably nonfunctional) form of the V2 receptor could be demonstrated in variant cell line N
57 ng 35S-labeled antisense cRNA probes for the V2 receptor demonstrated strong labeling of both arcades
58 recruitment of beta-arrestins eliminated the V2 receptor-dependent blockade of beta2 receptor interna
59  data support roles for multiple vasopressin V2-receptor-dependent signaling pathways in the vasopres
60                             In contrast, the V2 receptor efficiently coupled to a Gpa1p/G alpha(s) hy
61                                          The V2 receptor expressed in transfected cells labeled with
62 otypical G(s)-coupled receptor, we generated V2 receptor-expressing yeast strains (Saccharomyces cere
63 e nonpeptide antagonists to both the V1a and V2 receptors for AVP now allows for testing the hypothes
64 ly analyzed the ability of N- and C-terminal V2 receptor fragments to interfere with the activity of
65 ions C-terminal of Met(145) had no effect on V2 receptor function.
66 olecular basis underlying the selectivity of V2 receptor/G protein interactions, we used receptor sat
67 llular fractionation revealed that wild type V2 receptors generated a larger pool of cytosolic phosph
68 the novel observation that the efficiency of V2 receptor/Gs coupling can be modulated by the length o
69 s found to make an important contribution to V2 receptor/Gs coupling selectivity.
70 tion of the second intracellular loop of the V2 receptor had pronounced effects on receptor/G protein
71                                              V2 receptors heterologously expressed in yeast were unab
72 vasopressin and up-regulation of vasopressin V2 receptors in ADPKD.
73  tubular reabsorption of water by binding to V2 receptors in the renal collecting ducts, resulting in
74  but may involve transient downregulation of V2 receptors induced by exposure to supraphysiological d
75 ta2 receptors caused no detectable effect on V2 receptor internalization in the same cells.
76         Functional engagement of vasopressin V2 receptors is reported to produce rises in cAMP and ac
77                 We conclude that vasopressin V2 receptors mediate the antidiuretic effects of oxytoci
78 tor-selective and may cause hyponatremia via V2 receptor mediated antidiuresis.
79 ll, the findings support the conclusion that V2-receptor mediated signaling in collecting duct cells
80 ylyl cyclase, without affecting forskolin or V2 receptor-mediated activation.
81 o the water retention in pregnancy through a V2 receptor-mediated effect.
82  2 or 3 (beta-arrestin 1 or 2) abolished the V2 receptor-mediated inhibition of beta2 receptor intern
83 ignaling pathways involved in the short-term V2-receptor-mediated response in cultured collecting duc
84 nts demonstrated substantial aquaporin-2 and V2 receptor mRNA in microdissected arcades.
85 in after internalization of either wild type V2 receptor or its recycling mutant, indicating that lon
86 ctivity upon co-expression with a C-terminal V2 receptor peptide spanning the sequence where the vari
87 ine-vasopressin (AVP) binding to vasopressin V2 receptors promotes redistribution of the water channe
88 f this receptor region showed that two polar V2 receptor residues, Gln225 and Glu231, play key roles
89 y arginine vasopressin (AVP), which binds to V2 receptors, resulting in protein kinase A (PKA) activa
90 alpha(s) sequence (Gs5), indicating that the V2 receptor retained proper G protein coupling selectivi
91 e Gs, we systematically substituted distinct V2 receptor segments (or single amino acids) into the V1
92 arginine)-vasopressin (dDAVP), a vasopressin V2 receptor-selective agonist, for 7 d into Brattleboro
93 n COS-7 cells indicated that the presence of V2 receptor sequence at the N terminus of the third intr
94 hand, only those hybrid receptors containing V2 receptor sequence in the third intracellular loop wer
95              We administered desmopressin, a V2 receptor-specific agonist, to wild-type mice, SPAK-de
96                                          The V2 receptor-specific vasopressin analog dDAVP increased
97 le to form heterodimers with the full-length V2 receptor, suggesting that complex formation between m
98                      Third, mutations of the V2 receptor that block endomembrane recruitment of beta-
99 hortened, "diabetic" form of the vasopressin V2 receptor that is the product of incomplete posttransc
100 ation-dependent retention signal generated a V2 receptor that was recycled via the same compartment.
101 AVP) affects kidney function via vasopressin V2 receptors that are linked to activation of adenylyl c
102 eceptor, neurotensin receptor 1, vasopressin V2 receptor, thyrotropin-releasing hormone receptor, and
103 domain overrides the natural tendency of the V2 receptor to recycle and, by preventing its exit from
104 ructural basis underlying the ability of the V2 receptor to selectively recognize Gs, we systematical
105     These results indicate that AVP, via the V2 receptor, triggers a calcium signalling cascade obser
106 , immunoblotting experiments showed that all V2 receptor truncation mutants displaying dominant negat
107                           Several N-terminal V2 receptor truncation mutants were identified that stro
108 mplex formation between mutant and wild-type V2 receptors underlies the observed inhibition of wild-t
109 es for arginine vasopressin (AVP) within its V2 -receptor (V2 R).
110 that co-targeting two GPCRs, the vasopressin V2 receptor (V2R) and the calcium sensing receptor, usin
111 ist-induced internalization, the vasopressin V2 receptor (V2R) does not recycle to the plasma membran
112 The seven-transmembrane-spanning vasopressin V2 receptor (V2R) is a Gs-coupled receptor that is rapid
113 and resensitize rapidly, and the vasopressin V2 receptor (V2R), known to recycle and resensitize slow
114                     OPC-31260, a vasopressin V2 receptor (VPV2) antagonist, was shown to lower renal
115                              The vasopressin V2 receptor (VPV2R) antagonist OPC31260 has been effecti
116 uman disorders to test whether a vasopressin V2 receptor (VPV2R) antagonist, OPC31260, would be effec
117 cess was interrupted, the trafficking of the V2 receptor was compared with that of the recycling V1a
118                                    Thus, the V2 receptor was sequestered in the perinuclear recycling
119 ergic, angiotensin II type 1 and vasopressin V2 receptors was altered by the beta-arrestin-2 T178D mu
120 tant receptors, in contrast to the wild-type V2 receptor, was able to bind detectable amounts of the
121      Furthermore, the V2 beta 2, but not the V2 receptor, was capable of eliciting a mitogenic respon
122  found that angiotensin AT1a and vasopressin V2 receptors, which form stable receptor-beta-arrestin c

 
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