Relevant bibliographies by topics / Vasopressin receptor antagonist

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Academic literature on the topic 'Vasopressin receptor antagonist'

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Published: 5 June 2025
Last updated: 25 June 2025

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Journal articles on the topic "Vasopressin receptor antagonist"

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Burrell, Louise M., Paddy A. Phillips, K. A. Rolls, B. F. Buxton, C. I. Johnston, and J. J. Liu. "Vascular Responses to Vasopressin Antagonists in Man and Rat." Clinical Science 87, no. 4 (1994): 389–95. http://dx.doi.org/10.1042/cs0870389.

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1. The effects of the non-peptide arginine vasopressin V1 receptor antagonist (OPC-21268) and the non-peptide V2 receptor antagonist (OPC-31260) on vasopressin-induced contraction of human internal mammary arteries and rat mesenteric resistance arteries were investigated. 2. In human internal mammary arteries, the non-peptide V1 receptor antagonist, OPC-21268, failed to antagonize vasopressin-induced contraction at low concentrations and potentiated the contraction at higher concentrations (300 nmol/l, P < 0.05). A peptide selective V1 receptor antagonist {[d(CH2)5, sarcosine7]arginine vasopressin} potently inhibited the vasopressin-induced contraction, indicating the presence of functionally constrictor V1 receptors in human internal mammary arteries. Both peptide (desGly-NH29[d(CH2)5, D-Ile2, Ile4]arginine vasopressin) and non-peptide ‘selective’ V2 receptor antagonists (OPC-31260, 3 μmol/l) significantly antagonized vasopressin-induced contraction (P < 0.01), indicating partial V1 receptor antagonist activity. 3. The vasopressin-induced contraction in human internal mammary arteries was reversed by high concentrations of the non-peptide V2 receptor antagonist, OPC-31260, but not by the non-peptide V1 receptor antagonist, OPC-21268. 5. In rat mesenteric resistance arteries, both OPC-21268 (10 nmol/l) and OPC-31260 (1 μmol/l) antagonized vasopressin-induced contraction (P < 0.01). 6. The results of this study in vitro indicate that in human internal mammary arteries, the non-peptide OPC-21268 is a partial V1 receptor agonist with no V1 receptor antagonist activity, whereas the non-peptide OPC-31260 acts as a V1 receptor antagonist. Both OPC-21268 and OPC-31260 have V1 receptor antagonistic activity in vitro in the rat mesenteric resistance arteries. 7. These findings illustrate the complexity of the vasopressin receptor system and highlight the variability in results with peptide or non-peptide vasopressin analogues, between studies in vivo or in vitro, between species and across vascular beds.
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Liu, James J., Joan R. Chen, Brian B. Buxton, Colin I. Johnston, and Louise M. Burrell. "Potent Inhibitory Effect of Sr 49059, An Orally Active Non-Peptide Vasopressin via Receptor Antagonist, on Human Arterial Coronary Bypass Graft." Clinical Science 89, no. 5 (1995): 481–85. http://dx.doi.org/10.1042/cs0890481.

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1. The effect of vasopressin receptor antagonists varies between analogues (peptide, non-peptide) and across species. In this study the effect of the novel non-peptide vasopressin V1a receptor antagonist SR 49059 on human internal mammary arteries was investigated. 2. SR 49059 produced a potent, concentration-dependent, inhibitory effect on vasopressin-induced contraction of human coronary bypass graft internal mammary arteries. Both SR 49059 (1 μmol/l) and a peptide selective V1a antagonist {[d(CH2)5sarcosine7]arginine vasopressin} (1 μmol/l) abolished vasopressin-induced contraction. The non-peptide V1a receptor antagonist OPC-21268 (1 μmol/l) had no effect on vasopressin-induced contraction. 3. The effect of SR 49059 was specific to vascular vasopressin receptors as noradrenaline-induced contraction was not influenced by SR 49059. 4. The results of this study in vitro indicate that the non-peptide SR 49059 is a potent, specific vasopressin V1a receptor antagonist in the human internal mammary artery and suggest that it may be a useful tool for studying the pathophysiological role of vasopressin in man.
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Buckingham, J. C. "Vasopressin receptors influencing the secretion of ACTH by the rat adenohypophysis." Journal of Endocrinology 113, no. 3 (1987): 389–96. http://dx.doi.org/10.1677/joe.0.1130389.

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ABSTRACT The effects of selective agonists and antagonists of type 1 (V1) and type 2 (V2) vasopressin receptors on the secretion of ACTH in vitro by segments of adenohypophysial tissue and in vivo in rats pretreated with pentobarbitone and chlorpromazine were studied in the presence and absence of the 41 amino acid-containing peptide, corticotrophin-releasing factor-41 (CRF-41). The non-selective vasopressin receptor agonist, arginine vasopressin (AVP) and the V1-receptor agonist, felypressin caused dose-related increases in ACTH release in vivo and in vitro but the V2-receptor agonist, desmopressin was only weakly active in this respect. Their actions in vitro were antagonized competitively by the V1-receptor antagonist, d(C2H5)2-AVP, but were unaffected by the V2-receptor antagonist, d(CH2)5-d-Iso2-Thr4-AVP. Arginine vasopressin, felypressin and desmopressins in concentrations considerably lower than those necessary to elicit directly the release of ACTH, potentiated, in a dose-related manner, the activity of CRF-41 in vitro. The potentiating effects were not antagonized by the V2-receptor antagonist or by low concentrations of the V1 -receptor antagonist. At a higher concentration, the V1-receptor antagonist reduced, but did not abolish, the potentiating effects of AVP and its analogues. However, at this concentration, it also exhibited weak intrinsic activity and, like the agonists, potentiated the response to CRF-41. The results suggest that the direct effect of AVP on ACTH release is mediated by V1-like receptors. The vasopressin receptors involved in the potentiation of CRF-41 activity appear to be different. J. Endocr. (1987) 113, 389–396
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Kjær, Andreas, Ulrich Knigge, and Jørgen Warberg. "Histamine- and stress-induced prolactin secretion: importance of vasopressin V1- and V2-receptors." European Journal of Endocrinology 131, no. 4 (1994): 391–97. http://dx.doi.org/10.1530/eje.0.1310391.

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Kjær A, Knigge U, Warberg J. Histamine- and stress-induced prolactin secretion: importance of vasopressin V1- and V2-receptors. Eur J Endocrinol 1994;131:391–7. ISSN 0804–4643 We investigated the involvement of arginine vasopressin (AVP) V1- and V2-receptors in the prolactin (PRL) secretory response to histamine (HA) or restraint stress stimulation in conscious male rats by selective blockade of AVP receptors using different antagonists. Histamine (270 nmol) administered intracerebroventricularly or 5 min of restraint stress stimulated PRL secretion 10–14-fold. Pretreatment with the selective V1- receptor antagonists [1-(p-t-butyl-β-mercapto-β, β-cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-d-arginine] vasopressin or [1-(β-mercapto-β, β-cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-arginine]vasopressin inhibited the PRL response to HA and restraint stress in a dose-dependent manner with maximal inhibition of 60%. The effect of the two antagonists was identical when equipotent antivasopressor doses were administered. The selective V2-receptor antagonist [1-(β-mercapto-β, β-cyclopentamethylene propionic acid)-2-d-isoleucine-4-isoleucine-8-arginine]vasopressin was unable to inhibit the PRL response significantly. Combined administration of the V1-receptor antagonist [1-(p-t-butyl-β-mercapto-β, β-cyclopentamethylene propionic acid)-2-(O-methyl)tyrosine-8-d-arginine]vasopressin and the V2-receptor antagonist inhibited the PRL response to HA to the same extent as that observed when the V1antagonist was administered alone. None of the antagonists used had any effect on basal PRL secretion. We conclude that AVP seems to play a role in the mediation of HA- and restraint stressinduced secretion of PRL, and that the AVP receptor involved is primarily of the V1 -type or similar to this. Andreas Kjær, Department of Medical Physiology, Division of Endocrinology and Metabolism, The Panum Institute (Building 12.3), University of Copenhagen, Blegdamsvej 3, DK-2200 Copenhagen N, Denmark
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Flynn, Francis W., Thomas R. Kirchner, and Margaret E. Clinton. "Brain vasopressin and sodium appetite." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 282, no. 4 (2002): R1236—R1244. http://dx.doi.org/10.1152/ajpregu.00181.2001.

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Intraventricular injections of vasopressin (VP) and antagonists with varying degrees of specificity for the VP receptors were used to identify the action of endogenous brain VP on 0.3 M NaCl intake by sodium-deficient rats. Lateral ventricular injections of 100 ng and 1 μg VP caused barrel rotations and a dramatic decrease in NaCl intake by sodium-deficient rats and suppressed sucrose intake. Intraventricular injection of the V1/V2 receptor antagonist [d(CH2)5 1,O-Et-Tyr2,Val4, Arg8]VP and the V1 receptor antagonist [d(CH2)5 1,O-Me-Tyr2,Arg8]VP (MeT-AVP) significantly suppressed NaCl intake by sodium-deficient rats without causing motor disturbances. MeT-AVP had no effect on sucrose intake (0.1 M). In contrast, the selective V2 receptor antagonist had no significant effect on NaCl intake. Last, injections of 100 ng MeT-AVP decreased mean arterial blood pressure (MAP), whereas 100 ng VP elevated MAP and pretreatment with MeT-AVP blocked the pressor effect of VP. These results indicate that the effects produced by 100 ng MeT-AVP represent receptor antagonistic activity. These findings suggest that the effect of exogenous VP on salt intake is secondary to motor disruptions and that endogenous brain VP neurotransmission acting at V1 receptors plays a role in the arousal of salt appetite.
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Nakanishi, T., A. Yamauchi, H. Nakahama, et al. "Organic osmolytes in rat renal inner medulla are modulated by vasopressin V1 and/or V2 antagonists." American Journal of Physiology-Renal Physiology 267, no. 1 (1994): F146—F152. http://dx.doi.org/10.1152/ajprenal.1994.267.1.f146.

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For the purpose of clarifying the role of vasopressin V1 and V2 receptors in osmolyte accumulation, we determined the effects on the inner medullary osmolyte content of the administration of orally active vasopressin V1 and/or V2 receptor antagonists OPC-21268 (i.e., 1-(1-[4-(3-acetylaminopropoxy)benzoyl]-4-piperidyl)- 3,4-dihydro-2(1H)-quinolinone) and OPC-31260 (i.e., 5-dimethylamino-1-[4-(2-methylbenzoylamino)benzoyl]-2,3,4,5-tet rah ydro-1H- benzazepine] under a condition of maximal urine concentration achieved by water deprivation for 4 days. Taurine content increased significantly with the use of the V2 antagonist, irrespective of the use of the V1 antagonist. Inner medullary betaine content decreased with the administration of the V1 antagonist, irrespective of the administration of V2 antagonist. The administration of either the V1 or V2 antagonist alone did not affect sorbitol content, aldose reductase activity, or aldose reductase mRNA abundance in renal inner medulla. However, the combined administration of the V1 and V2 antagonists decreased all of these significantly. Myo-inositol content was not affected by the administration of the V1 or V2 antagonists. Glycerophosphorylcholine content was decreased with the use of the V2 antagonist, irrespective of the use of the V1 antagonist, and this effect paralleled urine osmolality. In conclusion, the individual organic osmolytes responded differently to the antagonists of vasopressin V1 and/or V2 receptors. The mechanisms linked to vasopressin V1 and/or V2 receptors appeared to modulate the accumulation of some organic osmolytes in the inner medulla. Aldose reductase mRNA abundance and sorbitol accumulation in the inner medulla appeared to be mediated through either V1 or V2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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Okada, H., H. Suzuki, Y. Kanno, Y. Yamamura, and T. Saruta. "Chronic and selective vasopressin blockade in spontaneously hypertensive rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 6 (1994): R1467—R1471. http://dx.doi.org/10.1152/ajpregu.1994.267.6.r1467.

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Chronic effects of orally available, nonpeptide vasopressin V1 and V2 receptor antagonists on conscious spontaneously hypertensive rats (SHR) were investigated. SHR and Wistar rats were divided into four groups, groups S-1 to S-4 and W-1 to W-4, respectively. Groups S-1 and W-1 were untreated as control. Groups S-2 and W-2 were treated with V1 antagonist, groups S-3 and W-3 received V2 antagonist, and groups S-4 and W-4 were treated with both of V1 and V2 antagonists. V1 and/or V2 antagonists did not affect degree of blood pressure of W-2, W-3, and W-4 rats, and V1 antagonist, alone or combined with V2 antagonist, slightly reduced increases in blood pressure of S-2 and S-4 rats without significance. However, V2 antagonist induced significantly massive and hyposmolar urine in W-3 rats compared with that in S-3 rats. In conclusion, in SHR, circulating vasopressin contributes to increases in blood pressure via either V1 or V2 receptors less than expected from previous studies with antibodies or peptide antagonists.
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Yang, Jia, Yehong Yang, Yongfei Wang, et al. "Role of Vasopressin Receptor 2 and 3 in ACTH-Secreting Tumors and their Potential Therapeutic Implications." Experimental and Clinical Endocrinology & Diabetes 128, no. 04 (2019): 263–69. http://dx.doi.org/10.1055/a-0808-4227.

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Abstract Purpose We investigated the expression of vasopressin receptor 2 and 3 on corticotrophin tumor cells, their role in regulating ACTH secretion, and their potential therapeutic implications. Methods We retrospectively assessed 52 hospitalized patients with pathologically confirmed ACTH-secreting tumors. The expression of vasopressin receptor 2 and 3 was explored via qualitative and quantitative immunohistochemistry analyses. The role of vasopressin receptors in regulating ACTH secretion was further studied in the AtT-20 cell line. Results Among 50 cases of pituitary corticotrophin adenoma, 31 were vasopressin receptor 2 positive, 38 were vasopressin receptor 3 positive, and 24 were both vasopressin receptor 2 and 3 positive. Two patients with ectopic ACTH syndrome were vasopressin receptor 3 positive, and one was also vasopressin receptor 2 positive. In 12 patients who underwent bilateral inferior petrosal sinus sampling before surgery, the central ACTH increment ratio after desmopressin stimulation was correlated with vasopressin receptor 2 but not with vasopressin receptor 3 staining intensity. In an in vitro study, the expression of both vasopressin receptor 2 and 3 on AtT-20 cells was confirmed. The vasopressin receptor 2 antagonist Tolvaptan inhibited desmopressin-induced ACTH secretion in a dose-dependent manner. Conclusions Both vasopressin receptor 2 and 3 are expressed in ACTH-secreting tumors. Vasopressin receptor 2 rather than vasopressin receptor 3 is the primary receptor that seems to mediate the ACTH response in corticotrophin tumors. A vasopressin receptor 2 antagonist can inhibit ACTH secretion induced by desmopressin in AtT-20 cells.
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Turner, M. R., and T. L. Pallone. "Vasopressin constricts outer medullary descending vasa recta isolated from rat kidneys." American Journal of Physiology-Renal Physiology 272, no. 1 (1997): F147—F151. http://dx.doi.org/10.1152/ajprenal.1997.272.1.f147.

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Arginine vasopressin (AVP) can selectively decrease blood flow in the renal medulla, but the sites of vasoconstriction are uncertain. We have examined the effects of vasopressin-receptor agonists and antagonists on the diameters of outer medullary descending vasa recta (OMDVR), isolated and perfused in vitro. AVP can constrict OMDVR, apparently via V1a-receptors. Ablumenal AVP (10(-10)-10(-6)M) or the selective V1a-receptor agonist [Phe2, Ile3, Orn8]-vasopressin (PO-VT, 10(-8) M) constricted OMDVR focally and (at higher AVP concentrations) transiently. The V1b agonist ideamino-Cys1,D-3-(pyridyl)Ala2,Arg8)vasopressin (DP-VP; 10(-8) M) and the V2 agonist [deamino-Cys1, D-Arg8]vasopressin (DDAVP; 10(-8) M) did not constrict OMDVR. The V1a antagonist [d(CH2)5(1), O-Me-Tyr2,Arg8]vasopressin (CTM-VP, 10(-10) 10(-8) M) inhibited vasoconstriction by AVP 10(-9 M), whereas the V2 antagonist [d(CH2)5(1), D-Ile2,Ile4 Arg8]vasopressin (II-VP) at low concentration (10(-10) M) did not. V2 stimulation seems to inhibit V1a constriction of OMDVR. DDAVP prevented constriction by PO-VT (10(-8) M) applied at the same time and dilated OMDVR preconstricted with PO-VT.
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Czaplewski, C., R. Kaźmierkiewicz, and J. Ciarkowski. "Molecular modelling of the vasopressin V2 receptor/antagonist interactions." Acta Biochimica Polonica 45, no. 1 (1998): 19–26. http://dx.doi.org/10.18388/abp.1998_4314.

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We predict some essential interactions between the V2 vasopressin renal receptor (V2R) and its selective peptide antagonist desGly9-[Mca1,D-Ile2,Ile4]AVP, and compare these predictions with the earlier ones for the non-peptide OPC-36120 antagonist- and the [Arg8]vasopressin (AVP) agonist-V2 receptor interactions. V2R controls antidiuresis in mammals and belongs to the superfamily of the heptahelical transmembrane (7TM) G protein-coupled receptors (GPCR)s. V2R was built, the ligands docked and the structures relaxed using advanced molecular modeling techniques. Both the agonist and the antagonists (no matter whether of peptide- or non-peptide type) appear to prefer a common V2R compartment for docking. The receptor amino-acid residues, potentially important in ligand binding, are mainly in the TM3-TM7 helices. A few of these residues are invariant for the whole GPCR superfamily while most of them are conserved in the subfamily of neurohypophyseal receptors, to which V2R belongs. Some of the equivalent residues in a related V1a receptor have been earlier reported as critical for the ligand affinity.
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Dissertations / Theses on the topic "Vasopressin receptor antagonist"

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Taveau, Christopher. "Rôle de la vasopressine dans les troubles du métabolisme glucidique : possible impact dans le développement du diabète." Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066211/document.

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Il est bien établi que la vasopressine (AVP) est élevée dans le diabète tant humain qu'expérimental. Chez l'homme, plusieurs études récentes ont montré une association entre la copeptine (biomarqueur de la sécrétion d'AVP), et la survenue d'un diabète ou d'une hyperglycémie, le syndrome métabolique et l'obésité. Dans l'équipe, nous avons montré une association inverse entre la consommation d'eau (diminue la sécrétion AVP) et le risque de survenue d'hyperglycémie dans la cohorte D.E.S.I.R. Le but de mon projet de thèse a été de déterminer le rôle de l'AVP et de la prise hydrique dans l'homéostasie glucidique chez le rat sain et dans un modèle de rat présentant un syndrome métabolique. L'administration aigüe ou chronique d'AVP augmente la glycémie et cet effet est réversé par un antagoniste des récepteurs V1a. L'activation des récepteurs V1b ne modifie pas l'insulino-sécrétion mais stimule en permanence et de façon modérée la glucagonémie. Ces effets ont été observés sur deux souches différentes de rats sains. Chez le rat Zucker obèse, l'AVP aggrave l'hyperinsulinémie à jeun et l'intolérance au glucose alors que le régime hydraté ne modifie pas la tolérance au glucose mais réduit très fortement la stéatose hépatique ainsi que le contenu hépatique en cholestérol et triglycérides et l'expression des gènes impliqués dans la lipogenèse. En conclusion, ces travaux montrent pour la première fois, que l'AVP dégrade à long terme la tolérance au glucose ; a contrario, un régime fortement hydraté est protecteur. Ces résultats, en accord avec nos données épidémiologiques, démontrent un lien de causalité entre vasopressine/hydratation et désordre du métabolisme glucidique<br>It is well established that vasopressin (AVP) level is high in both human and experimental diabetes. In humans, several recent studies have shown an association between copeptin (biomarker of AVP secretion) and the occurrence of diabetes mellitus or hyperglycemia, metabolic syndrome and obesity. Our team has shown a reverse association between water consumption (decrease AVP secretion) and the risk of hyperglycemia in the general population (D.E.S.I.R cohort). The aim of my thesis was to determine the role of AVP and fluid intake in glucose homeostasis in healthy rats and in a rat model of metabolic syndrome. AVP, administered acutely or chronically in healthy rats, increases glycaemia and this effect is reversed by a V1a receptor antagonist. V1b receptor activation does not influence insulin secretion but stimulates moderately basal glucagon production by the pancreas. These effects were observed in two different healthy strains of rats. In obese Zucker rats, a high AVP level worsens fasting hyperinsulinaemia and glucose intolerance whereas hydration does not affect glucose tolerance but drastically reduces hepatic steatosis, the content of cholesterol and triglycerides in liver and expression of genes involved in hepatic lipogenesis. In conclusion, these studies show for the first time, that AVP aggravates glucose tolerance whereas a highly hydrated diet is protective. These results, in agreement with our epidemiological data, demonstrate a causal link between vasopressin and/or hydration and glucose metabolism disorders
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Cotte, Nathalie. "Contribution de la pharmacologie moléculaire à l'étude des sites de liaison des récepteurs de la vasopressine." Montpellier 1, 1998. http://www.theses.fr/1998MON1T022.

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Tabrizchi, Reza. "Different modes of vasopressor actions of angiotensin and non-selective or selective beta-adrenoceptor antagonists." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/29439.

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Vasoconstriction can be initiated via the interaction of a number of chemicals with specific "receptive sites" known as the receptors. This thesis examines two distinctly different modes by which drugs initiate a contractile response, namely, (i) the interaction of angiotensin analogues with a heterogeneous population of angiotensin receptors in vascular smooth muscles, and (ii) the conditions whereby B-adrenoceptor antagonists interact with a-adrenoceptor antagonists thereby causing a pressor response. Conscious, unrestrained, instrumented-rats were used for the study. It has been suggested that angiotensin receptors in vascular and non-vascular tissues may not be of a homogeneous population. The first study examined whether a heterogeneous population of angiotensin receptors was responsible for increasing vascular tone. Dose-response curves were constructed for angiotensin II (ANG II) and des Asp¹ angiotensin II (ANG III) on mean arterial pressure (MAP) and mean circulatory filling pressure (MCFP), an index of total body venous tone, in the presence or absence of [Sar¹, Ile⁸]ANG II. The i.v. infusion of ANG II or ANG III caused dose-dependent increases in MAP and MCFP. In the presence of [Sar¹, Ile⁸]ANG II, the MAP and MCFP curves for ANG II were displaced to the right with pA₂ values of 9.2 and 8.4 for the arterioles and veins, respectively. However, the antagonist displaced dose-MCFP but not the dose-MAP response curve of ANG III. This suggests that ANG II and ANG III act on the same receptor in veins but not arterioles. This concept was further investigated by obtaining dose-MAP and dose-MCFP response curves for ANG II in the presence of ANG II or ANG III. Dose-MAP response curve to ANG II was displaced to the right in the presence of ANG II but not ANG III. Dose-MCFP response curve for ANG II was displaced to the right in the presence of ANG III but not ANG II. These results again suggest that ANG III acts on the same receptors as ANG II in the veins but not arterioles. In the last series of experiments two analogues of angiotensin III were compared as antagonists of the pressor response to ANG II and ANG III. In the presence of [Ile⁷]ANG III, the dose-MAP response curves for ANG II and ANG III were displaced to the right while in the presence of [Sar¹, Ile⁷]ANG III, the dose-MAP response curve for ANG III but not ANG II was displaced. This suggests that [Sar¹, Ile⁷]ANG III is a selective antagonist of ANG III in the arterioles. In summary, the results indicate that ANG III acts on a different sub-class of angiotensin receptors than ANG II in the arterioles but it may act as a partial agonist on the same type of receptors as ANG II in the venous bed. Thus, ANG II receptors in the arterioles appear to be different from those in veins. The administration of a non-selective β-antagonist propranolol into animals subjected to non-selective α-blockade has been observed to cause a paradoxical pressor response. This second study examines whether the paradoxical pressor response to β-antagonists was due to: (i) an interaction of a β-antagonist with an α-antagonist, (ii) blockade of vasodilator β₂-adrenoceptors or (iii) an increase in the release of catecholamines. Cumulative dose-response curves for propranolol, atenolol (β₁-antagonist) and ICI 118,551 (β₂-antagonist) were obtained in rats subjected to a continuous i.v. infusion of phentolamine, a non-selective α-antagonist. The administration of each of the β-antagonists caused a dose-dependent increase in MAP suggesting that the pressor response was not due to the blockade of vasodilator β₂-adrenoceptors. Another four groups of phentolamine-treated rats were given a single i.v. bolus injection of saline, propranolol, atenolol or ICI 118,551, and sampling of arterial blood for the determination of adrenaline (A) and noradrenaline (NA) concentration by HPLC/ec. Phentolamine caused a decrease in MAP and an increase in the plasma levels of A and NA. Subsequent injection of propranolol, atenolol and ICI 118,551 but not saline increased MAP. Neither saline nor any of the β-antagonists increased plasma NA or A levels suggesting that the pressor response was not associated with an acute increase in the release of catecholamines. It was also shown that prior injection of a β-antagonist partially antagonized the hypotensive effect of phentolamine suggesting that the pressor response was related to an interaction between α- and β-antagonists. It was further shown that a continuous infusion of either prazosin or rauwolseine caused a small but not significant decrease in MAP which was reversed by propranolol. Concurrent infusions of prazosin and rauwolscine caused a large decrease in MAP. Subsequent injection of propranolol caused a large pressor response. On the contrary, sodium nitroprusside or metha-choline each decreased MAP but the hypotension was not antagonized by propranolol. These results were consistent with the existence of a specific interaction between α- and β-antagonists. These experiments demonstrated that although the mechanisms involved in the initiation of a change in vascular tone did not share a common pathway, the final outcome shared a common denomination.<br>Medicine, Faculty of<br>Anesthesiology, Pharmacology and Therapeutics, Department of<br>Graduate
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Book chapters on the topic "Vasopressin receptor antagonist"

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Kagawa, Masahiro, Seigo Nagao, Tsuyoshi Kuniyoshi, et al. "Treatment of Vasogenic Brain Edema by V1 Receptor Antagonist of Arginine Vasopressin." In Recent Advances in Neurotraumatology. Springer Japan, 1993. http://dx.doi.org/10.1007/978-4-431-68231-8_60.

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Chan, Peter S., Joseph Coupet, Hyung C. Park, et al. "VPA-985, a Nonpeptide Orally Active and Selective Vasopressin V2 Receptor Antagonist." In Advances in Experimental Medicine and Biology. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4871-3_55.

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Nagao, Seigo, M. Kagawa, I. Bemana, et al. "Treatment of Vasogenic Brain Edema with Arginine Vasopressin Receptor Antagonist — an Experimental Study." In Brain Edema IX. Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9334-1_137.

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Kondo, Kazumi, and Yoshitaka Yamamura. "The Discovery of Samsca® (Tolvaptan): The First Oral Nonpeptide Vasopressin Receptor Antagonist." In Case Studies in Modern Drug Discovery and Development. John Wiley & Sons, Inc., 2012. http://dx.doi.org/10.1002/9781118219683.ch13.

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Bemana, Iraj, E. Takahashi, T. Nakamura, H. Kuyama, and S. Nagao. "OPC-21268, an Orally Effective, Nonpeptide Arginine Vasopressin V1 Receptor Antagonist Reduces Vasogenic Brain Edema." In Brain Edema X. Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6837-0_60.

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Patel, Mehul B., Ruediger W. Lehrich, and Arthur Greenberg. "Vasopressin Receptor Antagonists." In Hyponatremia. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6645-1_11.

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Brouard, R., V. Laporte, C. Serradeil Le Gal, et al. "Safety, Tolerability, and Pharmacokinetics of SR 49059, a V1A Vasopressin Receptor Antagonist, After Repeated Oral Administration in Healthy Volunteers." In Advances in Experimental Medicine and Biology. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4871-3_59.

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Irazabal, Maria V., and Vicente E. Torres. "Vasopressin Receptor Antagonism in PKD." In Polycystic Kidney Disease. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7784-0_13.

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Gal, C. Serradeil-Le. "Nonpeptide Antagonists for Vasopressin Receptors." In Advances in Experimental Medicine and Biology. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4871-3_54.

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Åkerlund, M., T. Bossmar, R. Brouard, and M. Steinwall. "Evidence for an Involvement of Vasopressin in Mechanism of Primary Dysmenorrhea and Effect of the Non-Peptide Vasopressin V1a Receptor Antagonist, SR 49059, on the Uterus of Non-Pregnant Women." In Advances in Experimental Medicine and Biology. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4871-3_60.

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Conference papers on the topic "Vasopressin receptor antagonist"

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Zhao, Ning, Stephanie Peacock, Chen Hao Lo, et al. "Abstract A063: Preclinical evaluation of an arginine vasopressin receptor 1A (AVPR1A) antagonist in castration-resistant prostate cancer." In Abstracts: AACR Special Conference: Prostate Cancer: Advances in Basic, Translational, and Clinical Research; December 2-5, 2017; Orlando, Florida. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.prca2017-a063.

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Moffat, Katrina J., and D. Euan MacIntyre. "REGULATION OF RECEPTOR-OPERATED Ca2− CHANNEL OPENING IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644677.

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Abstract:
Agonist-induced elevation of the platelet intracellular free Ca2+ concentration ([Ca2−]i), as monitored using quin2, is not electrically mediated and is attenuated by removal of extracellular Ca2− and by lanthanides (e.g Gd3−).Collectively these data suggest that elevation of [Ca2−]i in platelets derives in part via influx of external Ca2−presumably through a receptor-operated Ca2− channel (ROC). Hal lam &amp; Rink (FEBS Lett. 186: 175: 1985) showed that Mn2−also enters platelets via these ROC. To investigate the possible regulatory mechanisms that govern ROC status, we utilized quin2-labelled human platelets suspended in a Ca2+-free Hepes buffered Tyrodes solution, and monitored agonist-induced Mn2+-mediated quenching of quin2 fluorescence as an index of ROC opening.Thrombin (Th, 0.01-1 U/ml), Vasopressin (VP, 10-1000 nM) and the TxA2-mitnetic, EP171 (1-100 nM) all induced ROC opening which occurred rapidly (&lt;30s), was maximal within 30-60s and thereafter declined. Gd3+ (≤2 mM) markedly impaired this Mn2ࢤ-mediated quenching of quin2 fluorescence induced by all 3 agonists. The adenylate cyclase stimulant PGD2 (3-3000 nM) and the guanylate cyclase stimulant sodium nitroprusside (0.01-10 μM) impaired ROC opening induced by Th (0.5 U/ml), VP (100 nM) and EP171 (25 nM) whether added to platelets ≤120sbefore or 30s after the agonists. In contrast, agents that selectively antagonize, at the receptor level, the effects of VP (e.g. d(CH2)5Tyr Me AVP, 10 ¼H) or EP171 (e.g.EP092, 250nM), or that inhibit the action of Th(e.g. Hirudin 1 U/ml)only impaired ROC opening when added to platelets simultaneously with or before the agonist.These results indicate that, although initiated by agonist-receptor interaction, maintenance of the open state of ROC in human platelets does not require continued receptor occupancy or activation by agonist. Moreover, besides acting to impair the transduction processes initiated following occupancy by agonist of platelet Vi, TP and Thrombin receptors, cAMP-and cGMP-dependent reactions also can terminate or otherwise limit opening of ROC.
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