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PubMed1984

Effects of lysine-vasopressin (LVP) and 1-deamino-8-D-arginine-vasopressin (dDAVP) upon electrical potential, short-circuit current and transepithelial D.C. resistance of the frog skin.

The synthetic analogue of vasopressin, 1-deamino-8-D-arginine-vasopressin (dDAVP), possesses a protracted antidiuretic activity while having practically no pressoric activity as compared to arginine-vasopressin (AVP) or lysine-vasopressin (LVP). The effects of LVP and dDAVP were studied on the frog skin (Rana temporaria) sodium transport as reflected by the short-circuit current (SCC) level, on an Ussing apparatus. The application two different equimolar doses of LVP or dDAVP (approx. 9.4 X 10(-8) mol X l-1 and 18.8 X 10(-8) mol X l-1 to the inner surface of the skin resulted in identical maximal increases of sodium transport. However, the maximum transport stimulation after the application of dDAVP was delayed by about 30 min as compared to the stimulation by LVP (P less than 0.01). In addition, a protracted recovery of SCC towards its original levels was observed in experiments with dDAVP application after the hormone removal (P less than 0.01). It is concluded that dDAVP stimulates Na+ transport through the frog skin despite its lacking pressoric activity. Thus, the natriferic activity of vasopressin is related to its antidiuretic rather than pressoric activity. Maximum increase in the sodium transport following dDAVP application was delayed and more protracted as compared to the effect of LVP.

Animals↗
PubMed1994

The effect of eight V2 vasopressin receptor mutations on stimulation of adenylyl cyclase and binding to vasopressin.

We previously identified six V2 vasopressin receptor mutations in five unrelated nephrogenic diabetes insipidus (NDI) families. In order to elucidate the effect of these mutations on the function of the V2 vasopressin receptor, we introduced these six and two additional, naturally occurring mutations into the V2 vasopressin receptor gene by in vitro mutagenesis. Five of the mutants (two frameshift, one nonsense, and two missense) failed to stimulate adenylyl cyclase due to their inability to bind vasopressin under the experimental conditions. In contrast, ligand binding and cAMP accumulation were normal for two other mutations, a A61V missense mutation and an in-frame deletion of four amino acids (Arg-247 to Gly-250), suggesting that they are not the cause of NDI in these families. The deletion mutation was found in a family in conjunction with a second mutation, R181C, which yielded a much reduced ligand-binding capacity. The KD of R181C was at least 26 times higher than that of the wild type. Further characterization by an immunofluorescent assay showed that the R181C mutant receptor is expressed and distributed on the cell surface in a manner similar to that of the wild type. This finding indicates that the inability of this mutant to stimulate adenylyl cyclase is caused by the reduced capacity for vasopressin binding and that the R181C mutation is responsible for NDI in this family.

Adenylyl Cyclases↗
PubMed1987

4-Proline and 4-hydroxyproline analogs of arginine vasopressin: role of the proline substitution in the two beta-turns of vasopressin.

[4-L-Proline]arginine vasopressin, [4-D-proline]arginine vasopressin, [4-hydroxyproline]arginine vasopressin and [4-proline, 7-hydroxyproline] arginine vasopressin were synthesized and found to have antidiuretic activities of 91 +/- 4, 1.7 +/- 0.2, 1.0 +/- 0.1 and 4.4 +/- 1.0 units/mg, respectively. None of these analogs exhibited a significant level of rat pressor activity. The observed activities of these and other analogs with substitutions at position 4 and/or 7 are discussed on the basis of hypotheses and data bearing on the solution conformation of vasopressins.

Animals↗
PubMed1985

Neurohypophyseal hormones as evolutionary tracers: identification of oxytocin, lysine vasopressin, and arginine vasopressin in two South American opossums (Didelphis marsupialis and Philander opossum).

The neurohypophyseal hormones of two South American opossums (Didelphis marsupialis and Philander opossum) were isolated by molecular sieving and preparative high-pressure liquid chromatography (HPLC). One oxytocin-like and two vasopressin-like peptides were found in each species. These peptides have been identified by their amino acid composition and by their retention time in HPLC. Oxytocin, lysine vasopressin, and arginine vasopressin have been characterized in both species. Lysine vasopressin is roughly as abundant as arginine vasopressin. Comparison is made with Australian marsupials Macropodidae and Phalangeridae, and possible evolutionary mechanisms are discussed.

Amino Acids↗
PubMedDate not supplied

Vasopressin and ethanol preference. I. Effects of vasopressin and the fragment DGAVP on altered ethanol preference in Brattleboro diabetes insipidus rats.

Preference for concentrations of ethanol between 2.2 and 10 percent versus tap water was studied in Brattleboro rats homozygous for diabetes insipidus (di/di), heterozygous (di/+) or normal (+/+). The di/di rats, totally lacking in vasopressin, had greatly reduced preference scores for all concentrations of ethanol. Their intake of ethanol (g/day) was higher than heterozygotes or normals, but only when 2.2 percent ethanol was offered as a choice. Administration of lysine vasopressin or the vasopressin fragment des-9-Glycinamide-[Arginine8] vasopressin (DGAVP) using osmotic minipumps enhanced ethanol preference scores, reduced ethanol (g/day) intake, and restored total daily fluid intake in di/di rats. When di/di and di/+ rats were first allowed to develop stable ethanol preference before treatment with DGAVP, the peptide had no effect on preference scores. Thus, no treatment was effective in dissociating polydipsia from reduced ethanol preference and increased ethanol intake. While these results cannot exclude a possible regulatory role for endogenous vasopressin in ethanol preference drinking, they more strongly suggest that reduced preference for ethanol and increased ethanol intake are epiphenomena secondary to a polydipsic state.

Alcohol Drinking↗
PubMedDate not supplied

New evidence for neuronal function of vasopressin: sympathetic mediation of intrathecal vasopressin-induced hypertension.

Intrathecal injection of arginine vasopressin in rats at a dose as small as 10 ng produced dose-dependent hypertension and tachycardia. Pretreatment with the ganglionic blocking agent Ecolid, alpha-adrenoceptor antagonist phenoxybenzamine or the monoamine depleting agent reserpine blocked this effect without affecting intravenous vasopressin-induced hypertension. Intracerebroventricular injection of arginine vasopressin also induced hypertension and tachycardia, but 600 ng was needed. Ecolid and phenoxybenzamine also abolished this effect. Reserpine was not tested. It is concluded that both intrathecal and intracerebroventricular vasopressin-induced hypertension appears to be mediated by the sympathetic system and that the spinal cord is more sensitive than the supraspinal sites to vasopressin in regulating autonomic functions.

Animals↗
PubMedDate not supplied

Circadian variations of vasopressin level and vasopressin-converting aminopeptidase activity in the rat pineal gland.

Vasopressin levels and vasopressin-converting aminopeptidase activity were measured in the rat pineal gland during the 24 hr light-dark cycle. A rhythmic variation in peptide levels and peptidase activity occurred. At the onset of light at 6.00 hr, the peptidase displayed a significant, short-lasting (approximately 3 hr) increase of about 35% in activity, while a decrease of 28% in pineal vasopressin levels was observed. The changes in peptidase activity and peptide level were not triggered by light per se, since they persisted to occur at the same time point in animals which were not exposed to light, indicating the circadian nature of the rhythmicity. These changes were specific to the pineal gland, since other tissues, like hippocampus and pituitary gland, did not show these daily variations. The data suggest a relationship between vasopressin levels and vasopressin-converting aminopeptidase activity.

Aminopeptidases↗
PubMedDate not supplied

Neonatal treatment with vasopressin antagonist dP[Tyr(Me)2]AVP, but not with vasopressin antagonist d(CH2)5[Tyr(Me)2]AVP, inhibits body and brain development and induces polyuria in the rat.

Two vasopressin antagonists, d(CH2)5[Tyr(Me)2]AVP and dP[Tyr(Me)2]AVP, were given to Wistar rats from postnatal day 1 to 21 in order to investigate the influence on development and later diuresis. The latter antagonist significantly reduced body growth from day 3 postnatally onwards. At postnatal day 35 body, total brain, cerebellar and kidney weights were significantly reduced compared with controls. Diuresis, measured at one month of age, was four- to five-fold higher than the control group. Combined treatment with vasopressin failed to abolish the weight disturbances or polyuria. However, animals treated with the vasopressin antagonist d(CH2)5[Tyr(Me)2]AVP did not show developmental or diuretic deficits. Allometric analysis of brain/body relationship of the young animals indicated a disturbance of brain development by dP[Tyr(Me)2]AVP. Although the body and brain growth retardation induced by dP[Tyr(Me)2]AVP supports the hypothesis of a role for vasopressin in brain ontogeny, it can also be the result of a nonAVP-related toxic effect, since it could not be prevented by concomitant treatment with vasopressin.

Animals↗
PubMed1983

Hormonally active arginine-vasopressin suppresses endotoxin-induced fever in rats: lack of effect of oxytocin and a behaviorally active vasopressin fragment.

Vasopressin and oxytocin modulate memory processes which effects are dissociated from the typical peripheral endocrine effects of these neuropeptides. Recently, vasopressin has been implicated in the regulation of body temperature. In view of this, experiments were designed to determine whether the antipyretic effect of vasopressin was related to the action of the neuropeptide on memory processes. Fever was induced in rats by intracerebroventricular (i.c.v.) injection of 10 ng bacterial endotoxin (ET), which resulted in a rapid rise in colonic temperature. A second i.c.v. injection 15 min after ET administration of graded amounts (0.01, 0,1, 1 and 100 ng) or arginine-vasopressin (AVP) suppresses ET-induced fever in a dose-dependent manner, 1 ng being the minimally effective amount. Equivalent amounts of des-9-glycinamide-arginine-vasopressin (DG-AVP) or oxytocin (OXT) were ineffective. Large amounts (1,000 ng) of the latter two peptides, however, transiently mimicked the effect of AVP. On one-trial learning passive avoidance behavior, the neurohypophyseal peptides exerted a completely different pattern of effects. AVP and DG-AVP induced a dose-dependent facilitation, while OXT resulted in a dose-dependent attenuation of passive avoidance behavior. These findings suggest that AVP-induced antipyresis is related to the hormonally active AVP and dissociated from the effects of neurohypophyseal hormones and hormone fragments on other CNS processes-like learning and memory.

Animals↗
PubMed1997

Syndrome of inappropriate antidiuresis without involving inappropriate secretion of vasopressin in an elderly woman: effect of intravenous administration of the nonpeptide vasopressin V2 receptor antagonist OPC-31260.

We describe a 78-year-old female patient with severe hyponatremia owing to inappropriate antidiuresis. Despite hyponatremia, the urinary sodium excretion persisted with urine osmolality exceeding plasma osmolality. Although a water load decreased plasma sodium concentration and osmolality, the patient excreted only 40% of the water load after 4 h without decreased urine sodium concentrations and osmolality. The plasma vasopressin levels relative to plasma osmolality were not inappropriately elevated. Intravenous administration of the selective nonpeptide vasopressin V2 antagonist OPC-31260 decreased sodium concentration and osmolality in urine to lower values than in plasma. Concomitantly, the urine volume excretion increased markedly. In addition, restriction of water or administration of demeclocycline improved plasma sodium and plasma vasopressin levels relative to plasma osmolality to be normal. The findings indicate that the inappropriate antidiuresis in this patient was related to hyperfunction of the arginine vasopressin V2 receptor in the kidney which is not due to inappropriately secreted vasopressin.

Aged↗
PubMed1983

Effects of arginine-8-vasopressin and 1-deamino-8-D-arginine-vasopressin on ACTH secretion in rats.

The corticotropin-releasing effect of arginine-8-vasopressin (AVP) has been compared to that of 1-deamino-8-D-arginine-vasopressin (dDAVP) in male rats of R-Amsterdam strain. AVP increased the level of ACTH and corticosterone in the peripheral blood in a dose-dependent manner. In contrast to AVP, a very potent antidiuretic agent dDAVP which is devoid of pressor activity had no effect on ACTH release and did not stimulate the secretion of corticosterone. It is concluded that CRF activity of vasopressin in vivo is related to its pressor activity. These data are in agreement with the previous findings of these authors demonstrating that dDAVP shows a very low affinity for vasopressin receptors of the cell membranes in the adenohypophysis.

Adrenocorticotropic Hormone↗
PubMed1988

Comparison between lysine vasopressin and a long-acting analogue (N alpha-triglycyl-lysine vasopressin) used as local hemostatic agents for conization.

Lysine vasopressin and a long-acting analogue N alpha-triglycyl-lysine vasopressin were compared in a prospective randomized double-blind study including 71 women undergoing cold knife conization of the uterine cervix. Hemodynamic and hemostatic variables were studied. N alpha-triglycyl-lysine vasopressin had the following advantages over lysine vasopressin: it gave significantly less skin pallor, becoming evident at a later stage during the operation. The diastolic blood pressure was significantly lower, as also was the incidence of postoperative hemorrhages. Factor VIII related antigen was lower. On the other hand reduction in heart rate (values before conization compared with values during conization) was more pronounced when N alpha-triglycyl-lysine vasopressin was used, but there was no difference in absolute values between the two groups during conization.

Cervix Uteri↗
PubMed1982

[Tritium-labeled reactive analogs of [1,6-alpha-aminosuberic acid, 8-arginine] vasopressin (deamino-dicarba-[8-arginine] vasopressin. synthesis and properties].

The synthesis of three reactive analogues of [1,6-alpha-aminosuberic acid, 8-arginine]-vasopressin ([Asu1,6,Arg8]vasopressin) is described. Two peptide hormone analogues contain in the p-position of Phe2 the azido or 3-(3-methyl-3-diazirinyl)propanoylamino residue, which can be converted by photoactivation into nitrenes and carbenes, respectively. The third derivative contains the chemically reactive (bromoacetyl)amino group in the same position. The analogues are prepared via the precursor [Asu1,6,Phe(pNH2)2,Arg8]vasopressin, which is obtained by peptide synthesis in solution. Modifications of the p-amino group of Phe(pNH2) give the reactive analogues. The analogue containing p-azidophenylalanine in Pos. 2 shows a similar high binding affinity for the antidiuretic receptor in bovine kidney as vasopressin. By iodination of the Phe(pNH2) residue, followed by catalytic dehalogenation, the 2-(p-amino-phenylalanine) analogue is labelled with tritium at a specific radioactivity of 16 Ci/mmol. It can be converted into the tritium-labelled 2-(p-azidophenylalanine) analogue without loss of binding affinity for vasopressin receptors.

Amino Acid Sequence↗
PubMed2006

Investigation of mechanism of desmopressin binding in vasopressin V2 receptor versus vasopressin V1a and oxytocin receptors: molecular dynamics simulation of the agonist-bound state in the membrane-aqueous system.

The vasopressin V2 receptor (V2R) belongs to the Class A G protein-coupled receptors (GPCRs). V2R is expressed in the renal collecting duct (CD), where it mediates the antidiuretic action of the neurohypophyseal hormone arginine vasopressin (CYFQNCPRG-NH2, AVP). Desmopressin ([1-deamino, 8-D]AVP, dDAVP) is strong selective V2R agonist with negligible pressor and uterotonic activity. In this paper, the interactions responsible for binding of dDAVP to vasopressin V2 receptor versus vasopressin V1a and oxytocin receptors has been examined. Three-dimensional activated models of the receptors were constructed using the multiple sequence alignment and the complex of activated rhodopsin with Gt(alpha) C-terminal peptide of transducin MII-Gt(alpha) (338-350) prototype (Slusarz, R.; Ciarkowski, J. Acta Biochim Pol 2004 51, 129-136) as a template. The 1-ns unconstrained molecular dynamics (MD) of receptor-dDAVP complexes immersed in the fully hydrated 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylcholine (POPC) membrane model was conducted in an Amber 7.0 force field. Highly conserved transmembrane residues have been proposed as being responsible for V2R activation and G protein coupling. Molecular mechanism of the dDAVP binding has been suggested. The internal water molecules involved in an intricate network of the hydrogen bonds inside the receptor cavity have been identified and their role in the stabilization of the agonist-bound state proposed.

Amino Acid Motifs↗
PubMed2006

Analysis of interactions responsible for vasopressin binding to human neurohypophyseal hormone receptors-molecular dynamics study of the activated receptor-vasopressin-G(alpha) systems.

Vasopressin (CYFQNCPRG-NH(2), AVP) is a semicyclic endogenous peptide, which exerts a variety of biological effects in mammals. The main physiological roles of AVP are the regulation of water balance and the control of blood pressure and adrenocorticotropin hormone (ACTH) secretion, mediated via three different subtypes of vasopressin receptors: V1a, V1b and V2 receptors (V1aR, V1bR and V2R, respectively). They are the members of the class A, G-protein-coupled receptors (GPCRs). AVP also modulates several behavioral and social functions. In this study, the interactions responsible for AVP binding to vasopressin V1a and V2 receptors versus the closely related oxytocin ([I3,L8]AVP, OT) receptor (OTR) have been investigated. Three-dimensional models of the activated receptors were constructed using multiple sequence alignment, followed by homology modeling using the complex of activated rhodopsin with Gt(alpha) C-terminal peptide of transducin MII-Gt(338-350) prototype as a template. AVP was docked into the receptor-G(alpha) systems. The three lowest-energy pairs of receptor-AVP-G(alpha) (two complexes per each receptor) were selected. The 1-ns unconstrained molecular dynamics (MD) of complexes embedded into the fully hydrated 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphatidylcholine (POPC) lipid bilayer was conducted in the AMBER 7.0 force field. Six relaxed receptor-AVP-G(alpha) models were obtained. The residues responsible for AVP binding to vasopressin receptors have been identified and a different mechanism of AVP binding to V2R than to V1aR has been proposed.

Amino Acid Sequence↗
PubMed1992

Vasopressin V1-antagonist increases the hydroosmotic response to arginine vasopressin in frog urinary bladder.

V1-antagonist, [Mca1, D-Phe2, Sar7] arginine vasopressin, at a concentration 0.5 nM to 5 nM increased hydroosmotic effect of 5 nM arginine vasopressin in frog urinary bladder. 1 nM V1-antagonist [Mca1, O-Me-Tyr2] arginine vasopressin does not changed hydroosmotic effect of 0.1 nM dibutyryl cAMP. We suggest that-both V1- and V2-receptors are present on epithelial cells of frog urinary bladder and that V1-receptors are involved in the modulation of the hydroosmotic effect of arginine vasopressin-mediated by V2-receptors. by V2-receptors.

Animals↗
PubMed1988

Vasopressin and 1-deamino-8-D-arginine-vasopressin (DDAVP) reduce elevated plasma catecholamine levels in rats with hypothalamic deafferentation.

1. Anterolateral cut (ALC) of the medial basal hypothalamus (MBH) in rats produces an elevation of plasma catecholamine levels, especially of norepinephrine (NE), in unstressed animals and a more pronounced rise of plasma NE levels in response to immobilization (IMO). Animals with ALC have a destroyed corresponding vasopressin (AVP) and other peptides containing innervation of the median eminence and the posterior pituitary, resulting in the prevention of increased AVP secretion during the early intervals of IMO. 2. The administration of AVP (Pitressin, 7 days, 1 IU per rat i.m.) or of 1-deamino-8-D-arginine-vasopressin (DDAVP), an AVP analogue without pressoric activity, taken in drinking water (about 100 micrograms per day) was almost equally potent in decreasing the elevated water consumption and plasma NE levels in unstressed rats with ALC. However, the stress-induced potentiation of plasma NE levels in rats with ALC was not influenced by AVP substitution and only partly reduced by DDAVP in the late IMO intervals. 3. The lack of circulating vasopressin is the main factor in the mechanism of increased activity of the sympathoadrenal system induced by ALC in unstressed rats. 4. The regulation of sympathoadrenal activity by vasopressin and DDAVP in rats with ALC seems to be mediated predominantly by V2-subtype receptors. 5. In stressed rats with ALC the potentiation of plasma NE levels was not reduced after AVP or DDAVP administration, suggesting that some addition regulatory mechanisms were involved.

Afferent Pathways↗
PubMed1984

A bivariate radioimmunoassay for arginine vasopressin and the synthetic antidiuretic agent 1-deamino-8-D-arginine vasopressin (desmopressin).

Pairs of radioimmunoassays, each of which include a two-dimensional matrix of standards, have been previously employed to resolve specificity problems in steroid immunoassay. In this study the bivariate radioimmunoassay principle has been applied to simultaneous measurement of plasma antidiuretic hormone, arginine vasopressin, and the synthetic antidiuretic agent 1-deamino-8-D-arginine vasopressin (desmopressin), by utilizing two arginine vasopressin antisera which show significantly different cross-reactivities with the synthetic analog. Data processing consists of mathematical representation of two curved dose-response surfaces followed by solution of this pair of nonlinear simultaneous equations for the unknown arginine vasopressin and desmopressin concentrations. Details of numerical procedures are given in the Appendix. The assay appears entirely adequate in terms of sensitivity, accuracy, and precision for measurement of these antidiuretic agents in clinical samples. No evidence of significant covariance in estimated concentrations could be detected but precision of estimation is (not unexpectedly) a function of the concentration of both agents. The plasma disappearance half-time of desmopressin (probably the second of a biphasic disappearance) was estimated as 37 min in one normal subject, which is in good agreement with a previously reported value of 30 min.

Arginine Vasopressin↗