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

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